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(Circulation. 2002;106:2873.)
© 2002 American Heart Association, Inc.
Brief Rapid Communications |
From the Departments of Radiology (N.R.M., S.D., W.V., J.W., J.B.) and Cardiology (L.H., F.E.R.), Gasthuisberg University Hospital, Leuven, Belgium.
Correspondence to Jan Bogaert MD, PhD, Department of Radiology, Gasthuisberg University Hospital, Herestraat 49, B-3000 Leuven, Belgium. E-mail Jan.Bogaert{at}uz.kuleuven.ac.be
| Abstract |
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Methods and Results In 57 patients with acute myocardial infarction, chronic myocardial infarction, or ischemic cardiomyopathy, MRI was performed to evaluate ventricular function (CINE-MRI) and to depict presence of myocardial necrosis and/or scarring and no-reflow areas (CE-MRI). All studies were analyzed for concomitant ventricular thrombi. CE-MRI depicted 12 mural thrombi (3.1±2.9 cm3), located in left ventricular (LV) apex or adherent to anteroseptum, presenting as black, well-defined structures surrounded by bright contrast-enhanced blood. Thrombus formation on CE-MRI was related to larger end-diastolic volumes; lower ejection fractions; the region of delayed enhancement and lowest wall motion score, especially in left anterior descending coronary artery territory; and LV aneurysm formation. On CINE-MRI, thrombi were found in 6 patients. Nonvisualized thrombi were usually small (mean size 1.2±0.7 cm3). TTE depicted thrombi in 5. Nonvisualized lesions were most frequently located in LV apex and had a larger size than nonvisualized lesions on CINE-MRI (3.0±3.2 cm3). In 3 patients with suspected apical thrombus on TTE, MRI was normal.
Conclusions CE-MRI is not only an excellent technique to depict myocardial necrosis and scar tissue in patients with ischemic heart disease, but this study also suggests a better identification of LV thrombi than with presently used clinical imaging modalities, such as TTE.
Key Words: magnetic resonance imaging thrombus echocardiography heart disease myocardial infarction
| Introduction |
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13% of patients.2 When LV thrombus is present, oral anticoagulation significantly reduces risk of embolization.3 Risk factors for developing LV thrombus are infarct location (ie, anterior MI), infarct size and extent, and impairment in global and regional LV function.1,4 In clinical practice LV thrombi are diagnosed by transthoracic echocardiography (TTE).5 Recent studies with contrast-enhanced (CE)-MRI have shown promising results in defining presence and extent of myocardial necrosis and scarring.68 Because injection of paramagnetic contrast material also enhances the ventricular blood pool, the purpose of the present study was to evaluate the role of CE-MRI in detecting ventricular thrombi in patients with ischemic heart disease.
| Methods |
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MRI Protocol
Studies were performed on a 1.5-T Intera system (Philips Medical Systems). CINE-MRI, with the use of breath-holdbalanced fast-field-echo (b-FFE) technique, was performed in cardiac short-axis, vertical, and horizontal long-axis plane. CE-MRI was performed after intravenous injection of gadolinium-DTPA (0.2 mmol/kg body weight) with 3D-T1-weighted turbo-field-echo (TFE) technique in similar imaging planes. The inversion pulse was adjusted to optimally suppress normal myocardial signal. Images were obtained every 3 to 5 minutes during 20 minutes after injection.
MRI Analysis
MRI studies were analyzed blinded to echocardiography results and patient identity. LV function was quantified on CINE-MRI. CE and CINE-MRI were regionally analyzed with coronary artery (left anterior descending coronary artery, left circumflex coronary artery, right coronary artery) perfusion areas, thereby dividing the LV into 17 segments.9 Regional wall motion was described as normal (score: 5), mild hypokinesia (score: 4), severe hypokinesia (score: 3), akinesia (score: 2), or dyskinesia (score: 1), taking into account the segment with the lowest score in each perfusion territory. CE-MRI studies were similarly analyzed for abnormal increases in myocardial signal intensity and presence of no-reflow zones. The latter were defined as nonenhancing zones in areas with delayed enhancement. MRI studies were analyzed to assess LV thrombi. Thrombi were identified as intracavitary masses, distinguishable from papillary muscles, muscular trabeculations, and chordae. If present, signal intensity, size, and location were defined. Criteria to differentiate mural thrombi from no-reflow zones included: (a) differences in location (intracavitary versus intramyocardial); (b) differences in contrast fill-in on consecutive CE-MRI acquisitions; and (c) differences in appearance (well defined with sharp peripheral borders versus patchy, inhomogeneous, or well-defined subendocardial zones gradually thinning toward the periphery).
Transthoracic Echocardiography
Patients received 2D-TTE within one day of MRI study, with a Vingmed System Five (General Electric), Vingmed Vivid7, or an Agilent Sonos5500. Studies were independently analyzed from MRI findings. Thrombus was defined as an echodense mass within LV cavity with margins distinct from LV wall and distinguishable from technical artifacts and papillary muscles in at least two different echocardiographic views.
Statistical Analysis
Results are shown as mean±SD. A probability value of <0.05 was considered as statistically significant. Unpaired Students t test was used to compare patients with and without thrombus on CE-MRI. An ANOVA test was used to compare presence or absence of thrombus in relation with regional wall motion.
| Results |
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Presence of regional dyskinesia or akinesia was associated with a significantly higher number of thrombi than mildly hypokinetic (P=0.0075 versus dyskinesia and P=0.023 versus akinesia) or normally contracting regions (P=0.0015 versus dyskinesia and P=0.0043 versus akinesia) but not compared with severe hypokinetic regions (P=0.074 versus dyskinesia and P=0.23 versus akinesia). Presence of myocardial enhancement was associated with a significantly higher number of adjacent thrombi than regions without enhancement (P=0.0024). As shown in Table 2, thrombus formation on CE-MRI was related to larger end-diastolic volumes, lower ejection fractions, delayed myocardial enhancement, low wall motion scores in left anterior descending coronary artery territory, and presence of apical aneurysm. In 11 of 12 patients, oral anticoagulation was subsequently started, and in 9 patients follow-up was available (Figure 2).
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| Discussion |
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Because of the lack of histopathological validation of CE-MRI findings, we compared patients with and without thrombus formation on CE-MRI. Presence of thrombi was significantly related to the region of most severe functional impairment and/or the region with myocardial enhancement (ie, infarction or scarring). It should be mentioned that the criteria to differentiate no-reflow zones from mural thrombi are not definite, and thus differentiation may not always be straightforward. Because fill-in of no-reflow zones might take an hour or more, this criterion is not always useful for general clinical studies with a limited imaging time. As found by Paydarfar et al, who used T1-weighted MRI before and after contrast administration, organized thrombi may show peripheral, inhomogeneous enhancement.10 Because CE-MRI uses an additional inversional pulse to suppress the signal of normal myocardium, the relaxation of thrombotic tissue will also be altered. Further research and histopathological correlation is needed to evaluate the role of CE-MRI to differentiate subacute from organized clots.
In conclusion, the present study results stress the unique position of CE-MRI to assess patients with ischemic heart disease. Not only can the impact of the ischemic event on myocardial morphology and function be precisely assessed, but a frequent complication such as thrombus formation can also be diagnosed on CE-MRI. Moreover, in combination with CINE-MRI, perfusion-MRI, and possibly in the near future, MRI of the coronary arteries, a more complete evaluation can be made with this single noninvasive technique.
| Footnotes |
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Received September 9, 2002; revision received October 17, 2002; accepted October 17, 2002.
| References |
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2. Greaves SC, Zhi G, Lee RT, et al. Incidence and natural history of left ventricular thrombus following anterior wall acute myocardial infarction. Am J Cardiol. 1997; 80: 442448.[CrossRef][Medline] [Order article via Infotrieve]
3. Vaitkus PT, Barnathan ES. Embolic potential, prevention and management of mural thrombus complicating anterior myocardial infarction: a meta-analysis. J Am Coll Cardiol. 1993; 22: 10041009.[Abstract]
4. Asinger RW, Mikell FL, Elsperger J, et al. Incidence of left-ventricular thrombosis after acute transmural myocardial infarction. N Engl J Med. 1981; 305: 297302.[Abstract]
5. Visser CA, Kan G, David GX, et al. Two-dimensional echocardiography in the diagnosis of left ventricular thrombus: a prospective study of 67 patients with anatomic validation. Chest. 1983; 83: 228232.
6. Simonetti OP, Kim RJ, Fieno DS, et al. An improved MR imaging technique for the visualization of myocardial infarction. Radiology. 2001; 218: 215223.
7. 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: 19922002.
8. 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: 14451453.
9. Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantification of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantification of Two-dimensional Echocardiograms. J Am Soc Echocardiogr. 1989; 2: 358367.[Medline] [Order article via Infotrieve]
10. Paydarfar D, Krieger D, Dib N, et al. In vivo magnetic resonance imaging and surgical histopathology of intracardiac masses: distinct features of subacute thrombi. Cardiology. 2001; 95: 4047.[CrossRef][Medline] [Order article via Infotrieve]
11. Stratton JR, Lighty GW Jr, Pearlman AS, et al. Detection of left ventricular thrombus by two-dimensional echocardiography: sensitivity, specificity and causes of uncertainty. Circulation. 1982; 66: 156166.
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