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Original Report |
1 Department of Radiology, Gasthuisberg University Hospital Leuven, Herestr. 49,
B-3000 Leuven, Belgium.
2 Department of Cardiology, Hôpital St. Anne, Ave. J. Graindor 66, 1070
Brussels, Belgium.
3 Department of Radiology, Erasmus University Hospital, Brussels, Lenniksebaan
808, 1070 Brussels, Belgium.
Received May 29, 2002;
accepted after revision August 9, 2002.
Address correspondence to J. Bogaert.
Abstract
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CONCLUSION. On late-enhancement MR imaging, the various types or patterns of enhancement found in patients with hypertrophic cardiomyopathy are related to differences in morphology and regional function. Enhancement in hypertrophied areas likely reflects the presence of abundant connective tissue, foci of myocardial necrosis, or a combination of both.
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MR imaging can be used to depict the morphology of myocardial abnormalities [4]; to assess regional and global ventricular function [5]; to depict outflow tract obstruction, mitral valve systolic anterior motion, and mitral regurgitation [6]; and to assess coronary flow reserve [3]. The advent of improved contrast-enhanced MR imaging techniques allows accurate depiction of necrosis in patients with acute myocardial infarctions and scarred, fibrotic tissue in patients with chronic myocardial infarctions. A similar approach can be used to examine patients with hypertrophic cardiomyopathy [7]. The rationale for using MR imaging for this purpose is as follows: Histology of hypertrophic cardiomyopathy is characterized not only by a myofibrillar disarray but also by an abnormal increase in connective tissue. Furthermore, patients with hypertrophic cardiomyopathy are prone to developing myocardial ischemia. A diagnostic approach that includes contrast-enhanced MR imaging may lead to a better understanding of reduced or preserved regional myocardial performance.
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MR Imaging
Studies were performed on a 1.5-T MR imaging unit (Intera CV; Philips
Medical Systems, Best, The Netherlands) using Powertrak 6000 (Philips Medical
Systems) gradients (30 mT/m, 220-µsec rise time), a dedicated cardiac
software package, and the standard five-element Synergy cardiac coil with the
Vectorcardiogram option (Philips Medical Systems). After obtaining survey
images to localize the heart, we determined the cardiac axes with real-time
interactive MR imaging. Cine MR imaging was performed in the cardiac
short-axis, vertical long-axis, and horizontal long-axis planes and along the
left ventricular outflow tract, using a breath-hold balanced fast field-echo
sequence (TR/TE, 2.7/1.4; flip angle, 55°; field of view, 350 mm; matrix,
180 x 256; slice thickness, 8 mm; temporal resolution, 42 msec). The
cardiac short-axis slices encompassed the entire left ventricle.
Contrast-enhanced MR imaging was performed after administration of
gadopentetate dimeglumine (total dose of 0.2 mmol/kg of body weight) to
generate sufficient contrast between the normal and abnormal myocardium. We
used a three-dimensional T1-weighted turbo field-echo technique (4.1/2.1; flip
angle, 15°; field of view, 350 mm; matrix, 192 x 256; reconstructed
slice thickness, 10 mm; inversion time, 200–300 msec) in the cardiac
short-axis, vertical long-axis, and horizontal long-axis planes. For 20 min
after the injection of contrast material, we obtained images every 3–5
min.
Imaging Analysis
All images were sent to an off-line workstation for analysis. Global left
ventricular function was quantified, using a semiautomated delineation program
that provided the end-diastolic and end-systolic volume, stroke volume,
ejection fraction, and left ventricular myocardial mass. End diastole was
defined as the first image obtained 23 msec after the onset of the R wave of
the QRS complex. End systole was defined as the point during the cardiac cycle
at which the left ventricular cavity was the smallest. Adding all the volumes
of the individual slides yielded the global end-diastolic and end-systolic
volumes. We determined the myocardial mass by multiplying the myocardial
volume with the specific myocardial weight (i.e., 1.05 g/mL). End-systolic
volumes were adjusted for ventricular long-axis shortening, which was
accomplished by eliminating from calculation the basal slices encompassing the
left atrium at end systole. Subsequently, stroke volumes and ejection
fractions were calculated. End-diastolic thickness and systolic wall
thickening of the most thickened myocardial region were measured
perpendicularly through the wall.
We used late-enhancement MR imaging to assess the myocardium for an abnormal increase in signal intensity. If an abnormal increase in signal intensity was present, its location and extent were defined (subendocardial, mid wall, subepicardial, or transmural), the intensity of the enhancement was graded (weak, moderate, or strong), and its appearance was described (homogeneous or scattered).
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Imaging Findings
Of the 11 patients, eight had an asymmetric septal hypertrophy, two had a
concentric hypertrophy, and one had an apical hypertrophy. In eight patients
with the asymmetric septal form, the hypertrophy was located in the basal
region of the heart in three and in the basal to midventricular region in five
patients. Of these eight patients, three patients presented with a slight to
moderate outflow tract obstruction confirmed on echo Doppler sonography. One
patient had a concomitant mitral valve systolic anterior motion with mitral
regurgitation. Another patient with concentric hypertrophic cardiomyopathy had
a mild mitral regurgitation.
Global left ventricular function and mass calculations yielded a mean ± SD for end-diastolic volume of 99.5 ± 42.3 mL, a stroke volume of 69.4 ± 36.4 mL, an ejection fraction of 71.4% ± 7%, and a left ventricular mass of 159 ± 56 g. Although patients with myocardial enhancement yielded higher values than the unenhancing group, the statistical significance was difficult to assess because of the small sample size of the group. Measurement of the maximal end-diastolic wall thickness yielded a mean wall thickness of 23.1 ± 8.4 mm (range, 11–32 mm). The lowest value was obtained in a 10-year-old girl with a moderate concentric hypertrophy.
Abnormal myocardial enhancement was found in seven patients, and its location always corresponded to the most hypertrophied part of the myocardium (Fig. 1A, 1B, 1C). Enhancement was present 3 min after contrast injection and persisted during a 20-min period with no visual changes in enhancement size noted. Enhancement was patchy in five patients and homogeneous in two patients. In six patients, the intensity of enhancement was scored as strong in six patients and as weak in one patient. The extent of enhancement was always smaller than the extent of myocardial hypertrophy. Transmurally, enhancement involved more than two thirds of the wall in six of the seven patients. Figure 2A, 2B shows an apical hypertrophic cardiomyopathy in a 77-year-old woman that presented on ECG with negative giant T waves in the anterior leads.
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As shown in the graph in Figure 3, patients with myocardial enhancement had significantly thicker walls than those without myocardial enhancement, 27.8 ± 6.1 mm versus 14.7 ± 3.9 mm, respectively (p = 0.0042), whereas systolic wall thickening in patients with enhancement was significantly less than in those without enhancement, 1.9 ± 2.0 mm versus 6.3 ± 1.5 mm, respectively (p = 0.0046). This phenomenon is illustrated in Figures 4A, 4B, 4C and 5A, 5B, 5C. The patient in Figure 4A, 4B, 4C presented with significant wall thickening in the anterior and anteroseptal wall segments; imaging revealed strong myocardial enhancement and an almost completely abolished systolic wall thickening in the thickened zone. The patient in Figure 5A, 5B, 5C had less extensive wall thickening. After contrast injection, the myocardium displayed a somewhat inhomogeneous appearance overall, but no abnormal enhancement was found in the thickened regions. Regional function was well preserved in this area, as shown by the increase in wall thickness at end systole.
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Although use of gadopentetate dimeglumine has been previously reported in patients with hypertrophic cardiomyopathy [8, 9], those studies provided no information on functional parameters. Tsukihashi et al. [8] found either a homogeneous or a mixed isointense and hyperintense appearance of the hypertrophic myocardium. Koito et al. [9] related abnormal signal intensity to myocardial ischemia and related fibrosis to small-vessel disease or to myocardial degeneration and necrosis. In an experimental study by Aso et al. [10] in cardiomyopathic hamsters, areas displaying myocardial enhancement corresponded to areas with massive myocardial fibrosis, often showing a patchy or scattered appearance.
Since these studies were conducted, MR imaging sequences have been improved to allow better visualization of enhancement [11]. Addition of an inversion pulse to suppress the signal of normal myocardial tissues has yielded much higher contrast ratios between normal and diseased areas of the myocardium [7]. As in previous studies of patients with myocardial infarction, a dose of 0.2 mmol/kg of body weight of gadopentetate dimeglumine was used to generate sufficient contrast between normal and abnormal areas of the myocardium [7].
Our study results are in agreement with previously mentioned studies in patients and animal models. In most patients in our study, strong enhancement was found in the hypertrophied myocardium, occurring soon after injection and persisting for 20 min. Transmurally, the enhancement involved most of the myocardial wall and usually was scattered. This patchy enhancement likely reflects the presence of abundant connective (fibrotic) tissue intermingled with myofibrillar bundles in disarray in the hypertrophic myocardium. However, we cannot rule out the presence of concomitant ischemia-related necrosis as an explanation for the increased signal intensity and observed functional loss.
Ischemic necrosis, especially when caused by coronary artery disease, has a different distribution pattern, spreading in a centripetal fashion starting in the subendocardium, and if examined beyond the acute phase, the necrosis leads to a decrease in myocardial wall thickness [12]. Ischemic necrosis caused by intramyocardial microvascular obstruction can present in a more scattered way. Alterations in extracellular matrix composition and volume and in the wash-in and washout kinetics in these areas are likely the mechanisms responsible for the hyperenhancement. As a consequence of the loss in myocardial wall integrity, systolic wall thickening and thus regional function are impaired. We think that the reason that connective tissue changes were much less pronounced in our patients without myocardial enhancement was that those patients had less severe myofibrillar disarray, which would explain the findings that these regions are morphologically less affected and show a normal or better preserved systolic myocardial thickening.
The rarity of this disease led to a small sample size for our study, and that is its major limitation. Larger patient series are needed to further explore the precise relationship between myocardial enhancement and regional myocardial function. Moreover, techniques such as MR image tagging are needed to analyze the contribution of other components of regional contraction, such as circumferential or longitudinal shortening, but such techniques require sophisticated postprocessing. Finally, we have no histologic samples with which to prove our hypotheses. Endomyocardial biopsies in patients with hypertrophic cardiomyopathy are performed only to rule out diseases in specific heart muscles, such as cardiac amyloidosis. Myomectomy specimens from patients with left ventricular outflow tract obstruction were not available because none of the patients had a severe obstruction. Moreover, in our hospital, alcoholization of the first septal perforator is preferred to performing a myomectomy to treat these patients.
In conclusion, in our small patient group with hypertrophic cardiomyopathy, use of gadopentetate dimeglumine allowed us to define two groups with different regional performances of the hypertrophied myocardium. These findings might help to explain the conflicting results in the literature on preservation or decrease in regional myocardial performance.
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