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1 Department of Diagnostic and Interventional Radiology and Neuroradiology,
University Hospital Essen, Hufelandstrasse 55, 45122 Essen, Germany.
2 Department of Cardiology, West German Heart Center, University Hospital, 45122
Essen, Germany.
3 Department of Cardiology, Elisabeth Hospital, 45138 Essen, Germany.
Received June 21, 2004;
accepted after revision September 13, 2004.
Address correspondence to P. Hunold
(peter.hunold{at}uniessen.de).
Abstract
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MATERIALS AND METHODS. A total of 811 consecutive contrast-enhanced cardiac MRI studies performed for different indications were reviewed for left ventricular myocardial LE after gadopentetate dimeglumine administration. MRI studies were performed on a 1.5-T scanner using an inversion recovery turbo FLASH sequence (TR/TE, 8/4 msec; flip angle, 25°). The LE pattern of ischemic infarction scar was compared with that in nonischemic myocardial disease.
RESULTS. LE was found in 421 (52%) patients. In all patients with myocardial infarction, LE included the subendocardial layer. Nineteen patients without history of myocardial infarction and angiographically excluded coronary artery disease showed different patterns of LE caused by myocarditis, sarcoidosis, arrhythmogenic right ventricular dysplasia, cardiomyopathy, endomyocardial fibrosis, and iatrogenic scars after biopsy, ablation of septal hypertrophy, and myocardial laser revascularization.
CONCLUSION. LE in contrast-enhanced cardiac MRI is not specific for ischemic infarction. LE in ischemic infarction always involves the subendocardial layer, whereas it does not necessarily do so in other myocardial diseases. Therefore, if LE omits the subendocardial layer, different nonischemic myocardial diseases have to be considered. The pattern of LE might be helpful for the differential diagnosis of myocardial disease and in distinguishing it from ischemic disease.
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The purpose of the present study was to characterize myocardial LE in contrast-enhanced MRI caused by MI and to distinguish it from different entities of myocardial disease that are not related to acute or chronic ischemic MI.
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MRI
A 1.5-T scanner (Magnetom Sonata, Siemens Medical Solutions) was used for
all MRI examinations. The MRI protocol included a functional study of the left
ventricle (LV) using an ECG-triggered breath-hold segmented steady-state free
precession (SSFP; true fast imaging with steady-state free precession [FISP])
cine sequence (TR/TE, 3.0/1.5 msec; flip angle, 60°) with a slice
thickness of 8 mm. After three standard long-axis slices were obtained,
contiguous short-axis slices were acquired to cover the entire LV without an
interslice gap. Depending on the suspected or anticipated pathology (acute MI,
cardiomyopathy, inflammatory disease, etc.), T2 (TR, two R-R intervals; TE,
104 msec)-weighted turbo spin-echo (TSE) sequences were added in the long- and
selected short-axis views to assess myocardial edema.
After injection of 0.2 mmol/kg body weight of gadopentetate dimeglumine (Magnevist, Schering), LE scans were collected in three long-axis and all short-axis orientations by using a breath-hold ECG-triggered 2D inversion recovery turbo FLASH sequence (TR/TE, 8/4 msec; flip angle, 25°) as described previously [12]. Images were acquired subsequently up to 15 min after injection. The inversion time (TI, nonselective inversion pulse) was adjusted manually between 180 and 300 msec to null the signal of normal myocardium. Depending on the field of view, the typical in-plane resolution was 1.6 x 1.3 mm2 for all sequences. The total imaging time, including patient positioning, was 45–60 min.
Image Analysis
All MRI examinations were interpreted by two experienced radiologists
and/or cardiologists by consensus. True FISP images were reviewed as
cine-loops on a workstation, whereas hardcopies were used for the readout of
the TSE and inversion recovery turbo FLASH images. All data sets with LV
myocardial LE after gadopentetate dimeglumine were reviewed, and the
transmural extent (subendocardial, midmyocardial, subepicardial, and
transmural; Fig. 1) and pattern
(area, intensity, delineation, and distribution) of LE were evaluated. The
localization of LE within the LV was described by using the American Heart
Association's segmentation of the LV
[13].
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LE was judged to be of ischemic origin in patients with a history of MI
(suspicion of acute MI, known chronic MI, and signs of MI in ECG,
echocardiography, or nuclear imaging analyses) and/or proven CAD in coronary
catheter angiography (at least one coronary artery stenosis of 
70%). In
patients with angiographically excluded CAD and no history of MI, LE was
suggested to be caused by nonischemic disease. A comparison between
hyperintense areas in T2-weighted TSE images and the LE was performed
according to the above-described criteria. All entities of
non–infarction-related causes for LE were assessed, and the different
patterns of LE were related to the underlying pathology, as confirmed by a
final diagnosis based on clinical features, ECG (all patients), diagnostic
imaging (echocardiography, 644 patients; unenhanced MRI, seven patients;
nuclear imaging, 35 patients), and biopsy (six patients).
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LE in Myocardial Infarction
Of the 421 patients, 402 (95%) with LE had proven CAD, and 391 had a
history of MI. In 402 patients, 6,834 myocardial segments evaluated according
to the American Heart Association segmentation
[13] were assessed: 3,972
(58%) segments showed no LE. Nontransmural and transmural LE was found in
1,972 (29%) and 890 (13%) of the segments, retrospectively. In 26 (6%) of
these 402 patients, acute MI (onset of unstable angina < 2 weeks before)
was confirmed by high signal intensity in T2-weighted spin-echo images,
indicating myocardial edema. In 337 (84%) of 402 patients, MI had occurred
more than 6 months previously. Figure
2 shows a typical chronic subendocardial MI. LE in these groups
always included the subendocardial layer; isolated midmyocardial or
subepicardial LE was not found. Areas of high signal intensity in T2-weighted
images in patients with acute MI very closely matched the area of LE. In 12
patients, small areas of nontransmural LE were detected after coronary artery
stenting as described previously
[14].
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LE in Patients with Inflammatory Myocardial Disease
Six patients with inflammatory disease revealed LE. Patient 1
(Fig. 3), with acute
myocarditis, showed large areas of clearly demarcated LE that closely matched
the area and extent of hyperintense signal in the T2-weighted TSE sequences,
indicating edema. Patient 2, with chronic myocarditis, showed hypokinesis and
LE in segments 8, 9, 11, and 12 but normal signal intensity on T2-weighted
images unchanged in follow-up MRI after 3 months. Patient 3, with suspected
perimyocarditis in adolescence, showed a rim of sharply delineated LE in the
epicardial and mid portions of segments 5, 6, 9, 10, and 14. TSE images were
normal. The pattern of subepicardial LE with no clear distinction from the
adjacent pericardium suggests a prior occurrence of perimyocarditis
(Fig. 4). Patient 4, with known
perimyocarditis, had the same pattern of adherent myocardial and pericardial
LE in the inferior wall.
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Two patients with cardiac sarcoidosis presented with acute disease, impaired LV function, and atrioventricular block. Figure 5 (patient 5) shows multiple larger areas of LE in the turbo FLASH images. Patchy transmural LE mainly is found in the septal wall; however, there are areas with isolated subendocardial or subepicardial LE. T2-weighted TSE images revealed distinct hyperintensity in the areas of LE, indicating edema in acute inflammation. Patient 6 showed a similar pattern with LE and increased signal intensity on T2-weighted images.
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LE in Different Kinds of Cardiomyopathy
In nine patients, LE was found in cardiomyopathy. Patients 7 and 8 with
arrhythmogenic right ventricular cardiomyopathy presented with a grossly
dilated right ventricle and substantial thinning of the right ventricular free
wall. The right ventricular free wall showed transmural LE in larger areas.
Both of these patients had LV involvement with transmural LE in the lateral
wall. On T2-weighted TSE images, the signal intensity of these areas was not
different from that of normal myocardium. The pattern of LE could not clearly
be distinguished from that of ischemic MI due to the predominantly transmural
extent.
Four patients (patients 9–12) had hypertrophic cardiomyopathy (HCM) with LE in the LV myocardium. Patient 9 had some small spots of LE in segment 3 located in the middle of the wall. Figure 6 shows female patient 10 with severe symmetric LV hypertrophy. A diffuse pattern of LE in segments 7, 10–13, and 15 was seen, mainly localized in the central parts of the LV wall. Patients 11 and 12 displayed large, spotty areas of LE that were not clearly distinguished from the surrounding normal myocardium. In both patients, the subepicardial layer and the central wall of the intraventricular septum and the anterior wall were affected; the subendocardial layer did not enhance. None of these patients showed increased signal intensity on T2-weighted images.
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One patient (patient 13) had dilated cardiomyopathy (DCM) with the diagnosis based on severe dilation of the LV with impaired global function and no evidence of coronary sclerosis or occlusive CAD. LE was found in the basal and midventricular septum with the adjacent parts of the anterior wall and in the lateral wall. The pattern of LE was a thin, midmyocardial band with no involvement of the subendocardial layer.
Two patients showed endomyocardial fibrosis. One of them (patient 14) had only LV involvement and showed a 1-cm-thick layer of thrombus. A thin surface without perfusion and LE separated the thrombotic and/or fibrotic material from the blood pool. The other patient (patient 15, Fig. 7) had large thrombotic masses in the right and left ventricles. The thrombotic material in both patients had a similar pattern and time course of LE, that is to say, no early perfusion but homogeneous centripetal enhancement.
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Other Entities of LE
Patient 16, who had undergone transcoronary ablation of septal hypertrophy
(TASH) in hypertrophic obstructive cardiomyopathy (HOCM) 14 months earlier,
showed nontransmural LE as a surrogate of a septal scar after intervention,
which presented in the middle part and in the subepicardial portion of the
intraventricular septum (segment 9, Fig.
8).
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In patient 17, who had suspected acute myocarditis, an endomyocardial biopsy was taken, but it could not confirm inflammation. Two small dots (2 x 3 mm2) of LE could be detected in the subendocardial portion of the intraventricular septum 2 weeks after the biopsy, indicating the small biopsy lesion.
At 2 months after percutaneous transmyocardial laser revascularization (PMR) of the anterior wall in a patient (patient 18) with severe diffuse CAD, four small areas of LE could be detected in the subendocardial layer of the LV wall. Each of the scars representing laser channels after the intervention measured 6 mm in length and 2 mm in diameter.
A small area of transmural LE in the midventricular part of the septum (segment 8) was found in a young patient (patient 19) with paroxysmal tachycardia. The final diagnosis of this finding, however, could not be defined.
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After an accumulation of paramagnetic contrast agents in infarcted myocardium in animal models was reported in the early 1980s [15, 16], it was suggested that contrast-enhanced MRI might be feasible for the detection and quantification of MI. Recently, the concept of LE in gadolinium-enhanced MRI has emerged to become a standard technique for the evaluation of myocardial viability in CAD [1, 3–6, 17]. MI presents with either nontransmural LE, including the subendocardial layer, or transmural LE [4–6]. In the time course of MI, it has been shown that the extent of LE measured as a percentage of myocardial mass is larger in the acute than in the chronic stage [1]. This is due to the disappearance of contrast-enhanced edema over time in the nonnecrotic but reversibly damaged rim of infarction. In the area of cell necrosis that is transformed into fibrotic tissue, LE is irreversible.
Myocardial Inflammatory Disease
Gadolinium-enhanced MRI has been applied in inflammatory disease of the
myocardium [18]. Different
entities of myocardial inflammation have been shown to provide contrast
enhancement. In acute myocarditis and perimyocarditis and in chronic
lymphocytic myocarditis, areas of LE seem to represent a higher activity of
the inflammatory process [19,
20], and LE is reversible.
Friedrich et al. [11] applied
gadopentetate dimeglumine to monitor tissue changes in viral myocarditis and
found that MRI is able to localize and determine the activity and extent of
the inflammation by defining the area of enhancement using a T1-weighted
spin-echo sequence. Despite the anticipated presence of edema, none of the
patients in that study showed a significant intensity increase in the
T2-weighted imaging. LE was found in the subendocardial portions,
subepicardial portions, or the mid portions of the LV wall, but none of the
subjects showed transmural LE. These findings very closely match those of our
study, wherein no case of myocarditis or perimyocarditis showed transmural LE.
Therefore, the localization of LE might help in characterizing
myocarditis.
Our patients with cardiac sarcoidosis showed patchy, clearly demarcated, and very intense LE, which was partially transmural. The same pattern of LE was found in another study with T1-weighted spin-echo scans of six patients with proven cardiac involvement [21]. Rieker et al. [22] reported LE in 6 of 11 patients suffering from either acute myocarditis or sarcoidosis. Shimade et al. [23] reported LE in gadopentetate dimeglumineenhanced MRI in 8 of 16 patients with cardiac sarcoidosis, which diminished after therapy. In summary, contrast material might provide additional information for detecting and characterizing inflammatory tissue beyond T2-weighted spin-echo sequences.
Fibrotic Myocardial Disorders
Patients with secondary fibrotic tissue replacement and primary
cardiomyopathy may present with LE. In our four HCM patients, we found the LE
pattern, which has been found in animal
[10] and human
[24] studies to be
subepicardial or in the middle of the wall and not sharply delineated.
Dysfunction of the enhanced myocardial regions could be shown. In contrast,
our patients with DCM revealed a very sharp delineated band of midventricular
LE, which has very recently been described as pathognomonic for DCM
[25]. Generally, localization
of typical LE might help to distinguish cardiomyopathic disease from former
infarction. Although there are other MRI techniques for evaluating
cardiomyopathy [26], contrast
material seems to enhance the diagnostic capabilities.
Our two cases of endomyocardial fibrosis showed a very similar time course of LE with a centripetal accumulation over time. One case report is available with a similar contrast enhancement pattern in endomyocardial fibrosis [27]. Due to this pattern, the thrombus was classified as chronic with fibrotic tissue replacement [28]. LV involvement in right ventricular cardiomyopathy, as seen in two of our patients, has been reported previously. "Fibrofatty" wall replacement of the LV free wall has been reported because arrhythmogenic right ventricular cardiomyopathy seems to be a generalized cardiomyopathy [29, 30].
Iatrogenic Myocardial Changes After Therapy
Some interventional procedures are accompanied by scarring after a lesion
is set. TASH in HOCM patients leaves septal scars after an infarct is set
through occlusion of the septal branches of the left anterior descending
artery. In our case, the septal scar was not located in the region suggested
but was in the mid portion of the septum having no impact on the LV outflow
tract obstruction. Some literature is available on the use of MRI in the
follow-up of HOCM patients after TASH
[31]. In one case report, the
authors describe a pattern of LE after TASH that is very similar to that of
our patient, that is to say, subepicardial enhancement in the septum
[32].
Endomyocardial biopsy sets small areas of scars after a small part of the endomyocardium is torn apart. To our knowledge, these have not been described by in vivo imaging techniques thus far. PMR, which was introduced in therapy to initiate angiogenesis in end-stage CAD, causes small scar channels. Histopathologic examinations on PMR have shown channel remnants composed of granulation tissue, fibrosis, and new vessels as an unspecific reaction to tissue injury [33]. These "channels" seem to be visible by contrast-enhanced MRI due to the LE.
Clinical Implications
In conclusion, LE in cardiac MRI is not specific for MI. LE occurs in a
variety of myocardial disorders and can be diagnosed by using the turbo FLASH
technique. In MI scar, LE always involves the subendocardial layer. If, on the
other hand, LE omits the subendocardial layer, different nonischemic
myocardial diseases have to be considered. Therefore, the pattern and
distribution of LE within the myocardium might facilitate the differential
diagnosis of myocardial disease and allow ischemic and nonischemic myocardial
damage to be distinguished. Since nonischemic diseases causing LE are rare
compared with CAD, large trials are mandatory in order to understand the
pathophysiology and to distinguish the different enhancement patterns.
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