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Case Report |
1 Russell H. Morgan Department of Radiology and Radiological Sciences, Johns
Hopkins Hospital, Rm. 143, 600 N. Wolfe St., Baltimore, MD 21287.
2 Division of Cardiology, Department of Medicine, Johns Hopkins Hospital,
Baltimore, MD 21287.
Received November 28, 2001;
accepted after revision January 17, 2002.
Address correspondence to D. A. Bluemke.
Introduction
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Delayed gadolinium-enhanced MR imaging is a new method for assessing viable myocardium [4]. To our knowledge, we describe the first report of viability MR imaging to help characterize a left ventricular aneurysm that was indeterminate in type on the basis of echocardiography and ventriculography.
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The MR examination was performed with a 1.5-T MR imager (CV/i; General Electric Medical Systems, Waukesha, WI) using a dedicated cardiac coil. Steady-state free-precession gradient-echo short-axis and vertical long-axis images (TR/TE, 3.5/1.4; slice thickness, 8 mm; number of excitations, 1; matrix, 220 x 160; and field of view, 380 x 285 mm) were acquired. Double inversion recovery fast spin-echo short-axis images were also obtained (1071/31.4; slice thickness, 6 mm; number of excitations, 1; field of view, 360 x 270 mm; and matrix, 256 x 224). After IV administration of contrast material (0.2 mmol/kg of gadopentate dimeglumine), inversion recovery prepared breath-hold cine gradient-echo images (7.2/3.2; inversion time, 200 msec; flip angle, 25°; slice thickness, 10 mm; number of excitations, 2; matrix, 256 x 192; and field of view, 360 x 270 mm) were obtained 10 min after gadolinium injection.
Both the spin-echo (Fig. 1A) and cine (Fig. 1B) MR images revealed a focal outpouching in the anterior wall of the left ventricle. The outpouching was segmentally thin because of a focal loss of myocardium. The transition between the normal contractile myocardium and the aneurysm was abrupt. The mouth of the aneurysm was similar to the largest diameter of the aneurysm. Because the transition to the aneurysmal sac was abrupt, we believed that gadolinium-enhanced (viability) images would help to increase confidence in determining the aneurysm type. Contrast-enhanced delayed images showed transmural hyperintensity that corresponded exactly to the extent of the aneurysmal sac (Fig. 1C). Adjacent myocardium that was not part of the aneurysm showed no hyperenhancement (Fig. 1D). Because the region of delayed hyperenhancement involved only the area of myocardial scarring in the aneurysmal sac, the diagnosis of left ventricular true aneurysm associated with a prior myocardial infarction was established. Further evaluation of the patient's medical history revealed that she was hospitalized 2 years previously with acute onset of cardiac dysfunction and pulmonary edema. On the basis of the imaging findings, it was suspected that that was the time of the patient's initial myocardial infarction.
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Because the clinical distinction between a true aneurysm and a pseudoaneurysm is critical, additional assessment with various imaging modalities is required. A number of noninvasive diagnostic modalities have been used to detect left ventricular true aneurysms. Because persistence of ST-segment elevation and T-wave inversion appears to be a feature of both true aneurysms and pseudoaneurysms, ECG is not helpful in distinguishing between the two. On ECG, true aneurysms distort the shape of the left ventricle during both diastole and systole, and the motion of the aneurysmal segment is paradoxical. A true aneurysm has a wide neck, and the diameter of the neck is comparable with the maximal diameter of the aneurysm. Although echocardiography has the advantage of being noninvasive, it has some limitations such as occasional failure to characterize the neck of an aneurysm. One of the common imaging findings for differentiating true aneurysms from pseudoaneurysms is location, which may be identified on a conventional chest radiograph [3]. The presence of a discrete bulge in the heart anteriorly is suggestive of a true aneurysm. However, the bulge was not detected in our patient; therefore, further imaging was necessary.
MR imaging has an increasing potential in the noninvasive evaluation of patients with myocardial infarction and subsequent complications. MR imaging can clearly localize the site of the aneurysm [2]. Additional advantages include the capability to distinguish between pericardium, thrombus, and myocardium, which are not easily distinguished by contrast-enhanced ventriculography or cardiac catheterization. Viability MR imaging of the myocardium uses a delayed contrast-enhanced imaging technique to accurately delineate the infarct size and its extent. In the case of a true aneurysm, the tissue making up the wall of the aneurysm will show delayed enhancement, indicating scar tissue as a result of infarcted myocardial muscle. Because the wall of the pseudoaneurysm is composed only of pericardium, it does not show delayed enhancement in the sac; however, the border of the aneurysm will show enhancement, indicating a perianeurysmal infarcted area. In recent studies, contrast-enhanced MR imaging has shown the signal enhancement of nonviable, infarcted myocardium resulting from the accumulation of contrast material in both acute and chronic infarction [7, 8]. In acute infarction the presence of hyperenhancement corresponds to the regions of acute myocyte necrosis, whereas in chronic infarction the hyperenhancement correlates with scar tissue. On the basis of studies performed using contrast-enhanced delayed (>5 min) MR imaging, viable myocardium can easily be distinguished from nonviable myocardium as unhyperenhanced and hyperenhanced regions, respectively [8]. In patients with ischemic heart disease, a combination of cine and contrast-enhanced MR imaging adds diagnostic capability by allowing the examination of wall motion, the visualization of a wide orifice, and the distinction between myocardial scarring and viable myocardium that supports a diagnosis of left ventricular true aneurysm.
Delayed enhancement of the myocardium is not specific for a myocardial scar (fibrosis). For example, tumors and inflammatory disease have also been reported to show delayed myocardial enhancement. Enhancement of the pericardium related to a pseudoaneurysm has not been previously reported to our knowledge. However, that thrombus could form in an unruptured pseudoaneurysm with subsequent organization or revascularization that could result in delayed enhancement. Thus, the findings described in our case are not known to be entirely specific for true left ventricular aneurysm. Further experience with these techniques of delayed myocardial enhancement is needed to establish these findings with increased certainty.
In summary, we present a challenging case that shows the difficulty of verifying the diagnosis of left ventricular true aneurysm using conventional imaging. Our article suggests an important role for cardiac viability MR imaging for aneurysmal characterization and for improving confidence in the diagnosis.
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