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Cardiac Imaging |
1 From the Departments of Radiology (J.P.L., E.S.), Cardiology (F.H., L.J.F., J.M.J., P.G.S.), and Nuclear Medicine (M.F.), Hôpital Bichat, 46 rue Henri Huchard, 75877 Paris 18, France. From the 2003 RSNA Annual Meeting. Received August 4, 2004; revision requested October 8; revision received November 4; accepted December 14. Address correspondence to J.P.L. (e-mail: jean-pierre.laissy{at}bch.ap-hop-paris.fr).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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MATERIALS AND METHODS: All examinations were performed according to guidelines of the institutional board on medical ethics and clinical investigation and after informed patient consent was obtained. Fifty-five patients with a clinical presentation suggestive but not typical of AMI were examined. At final diagnosis, 31 patients had AMI and 24 had myocarditis. At-rest MR imaging was performed and included first-pass perfusion and delayed-enhancement sequences. Three independent observers read each image data set separately and then in consensus. The main abnormalities included first-pass perfusion defects and delayed highly enhancing areas. The numbers and distributions of involved segments and the transmural extents and the shapes of the highly enhancing areas were noted. For comparisons between the AMI and myocarditis patient groups, the 
2 test was used to assess the locations of the abnormalities and the Mann-Whitney U test was used to assess the numbers of involved segments. The final diagnoses were obtained with coronary angiography as the reference standard for the AMI group and on the basis of normal coronary angiographic findings and the spontaneous resolution of clinical symptoms and wall motion abnormalities for the myocarditis group.
RESULTS: MR imaging patterns were significantly different between the two cardiac disease groups (P < .05). All the patients with AMI had a segmental early subendocardial defect, with corresponding segmental subendocardial or transmural delayed high enhancement in a predominantly anteroseptal or inferior vascular distribution in 28 patients. All patients with AMI had stenosis of at least the infarct-affected coronary artery. All but one of the patients with myocarditis had no early defect and focal or diffuse nonsegmental nonsubendocardial delayed enhancement predominantly in an inferolateral location.
CONCLUSION: Use of combined early- and late-perfusion MR imaging sequences helps to distinguish AMI from myocarditis.
© RSNA, 2005
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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The formal differential diagnosis of AMI or acute myocarditis is based on positive findings of endomyocardial biopsy, which usually is considered the reference standard. However, this invasive procedure has several major drawbacks (2): First, the diagnostic sensitivity of endomyocardial biopsy strongly depends on the quality of the sample, and false-negative results can be observed when the sample is taken from a noninvolved area. Second, endomyocardial biopsy may have severe side effects, and the risk-to-benefit ratio may be questionable when the procedure is performed to determine the presence or absence of a disease, such as myocarditis, that appears to be benign and is spontaneously regressive in most cases. Third, there are no specific histologic criteria that can be used to reliably predict in the acute phase the (rare) occurrence of chronic myocarditis with progressive left ventricular dysfunction (3). Fourth, endomyocardial biopsy is not indicated for areas suspected of being affected by an ischemic process.
Although patients with acute myocarditis usually are younger and have fewer coronary risk factors compared with patients who have AMI (4), the clinical symptoms of acute myocarditis at presentation frequently necessitate emergency coronary angiography to exclude AMI. However, even when emergency coronary angiography is performed in patients suspected of having acute myocarditis, it still may be difficult to distinguish AMI yielding normal coronary angiographic findings (owing to temporary coronary artery occlusion and then spontaneous reperfusion or to prolonged coronary artery spasm) from acute myocarditis with segmental involvement. Therefore, an accurate noninvasive procedure to diagnose acute myocarditis is needed. Ideally, one would be able to repeat this procedure during follow-up to assess for the complete resolution of the inflammation.
Magnetic resonance (MR) imaging performed with specific T2-weighted and pre- and postcontrast T1-weighted sequences (5,6) has been shown to be promising for the detection of acute myocarditis; these sequences are particularly well suited for the examination of inflammatory disorders. With the advent of fast perfusion MR imaging modalities specifically designed for imaging AMIs, it is important to be able to assess the imaging patterns of myocarditis by using typical AMI imaging sequences. Thus, the purpose of our study was to prospectively determine whether early first-pass perfusion and delayed-enhancement MR imaging sequences can enable the differentiation of AMI from myocarditis in patients with acute chest pain.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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The patients involved in this study represent the aggregate of two populations: The first group comprised 31 patients with AMI who were randomly selected from our overall population of patients with myocardial infarction; all of these patients had significant coronary artery stenosis (>50% luminal narrowing) at coronary angiography. The second group comprised 24 additional patients who were consecutively referred to our imaging department during the same time period because they were suspected of having myocarditis rather than AMI. All of these patients had undergone coronary angiography before MR imaging, and none had angiographic findings suggestive of an acute coronary syndrome; however, one of them did have mild coronary artery disease. These patients were not matched to the patients with AMI, and this explains the difference in baseline characteristics between the two populations.
All patients included in the study had undergone emergency coronary angiography at admission. The patients were recruited after they had undergone coronary angiography, but the recruiting cardiologist was unaware of the angiographic results. The overall exclusion criteria were cardiogenic shock, hemodynamic instability, severe congestive heart failure, ventricular tachyarrhythmia, any contraindication to MR imaging, and/or unwillingness to participate in the study. All imaging examinations were performed according to the guidelines of our institution's board on medical ethics and clinical investigation. Informed consent was obtained from all patients, as required by our institutional review board.
The final diagnosis of AMI—in 31 patients—was made when the patient at presentation had chest pain, ECG changes suggestive of myocardial ischemia or infarction, and elevated biochemical markers and was found to have significant coronary artery disease (<50% coronary artery stenosis) in the same vascular territory in which the ECG and/or echographic wall motion abnormalities were located. In addition, 23 (74%) of these 31 patients had a clearly identifiable culprit artery and seven (23%) had a history of coronary artery disease, with myocardial ischemia having been documented at previously performed stress and at-rest scintigraphy. Acute coronary reperfusion was performed by means of primary or rescue thrombolysis followed by percutaneous transluminal coronary angioplasty in 22 of these 31 patients. Twenty-one patients with AMI had single-vessel disease, and the remaining ten had multiple-vessel disease. Three patients had had a previous myocardial infarction an average of 5.4 years earlier. The infarct-affected arteries were assigned a TIMI (Thrombolysis in Myocardial Infarction) grade of 3 (n = 26) or 0–1 (n = 5) at initial coronary angiography.
Although the 24 patients with myocarditis also had chest pain and ECG abnormalities suggestive of myocardial ischemia or infarction at presentation, they received a diagnosis of myocarditis on the basis of normal coronary angiographic findings or owing to the presence of mild coronary artery disease (<50% coronary artery stenosis) with diffuse or nonmatched wall motion abnormalities (n = 24); a transient increase in biochemical markers of myocardial injury followed by a spontaneous resolution of clinical symptoms and of segmental or global wall motion abnormalities; and/or serologic changes compatible with recent viral infection based on the results of polymerase chain reaction performed to detect adenovirus, cytomegalovirus, enterovirus, Epstein-Barr virus, or influenza virus A or B (n = 3). Two patients with myocarditis had positive immunologic test results. Significant coronary artery stenosis or spontaneous coronary artery spasm at coronary angiography was a selective exclusion criterion for myocarditis.
Twenty-five men and six women had AMI, and 17 men and seven women had myocarditis (P = .53, 2 test); there was no significant difference in sex between the two groups. The mean ages of the patients with AMI and myocarditis were 59 years ± 1.9 (standard deviation) and 44 years ± 3.7, respectively (P = .001, analysis of variance). Other patient characteristics are given in Table 1.
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Cine steady-state free precession MR images were obtained by using the following parameters: 4.2/1.5 (repetition time msec/echo time msec), a 60° flip angle, a 310 x 310-mm field of view, a 224 x 224 matrix, a 7–8-mm section thickness, and approximately 35 phases per section, according to the cardiac frequency. Twelve views were shared per phase.
Myocardial first-pass perfusion data were acquired by using an ECG-gated T1-weighted multishot gradient-echo echo-planar inversion-recovery (IR) MR imaging sequence with interleaved notched saturation (6.6/1.3/240 [repetition time msec/echo time msec/inversion time msec], 25° flip angle). Five to eight 10-mm-thick short-axis sections (128 x 128 pixels in a 330-mm field of view) were acquired every two heartbeats. This sequence was typically repeated 35 times, according to the heart rate. A 3–4-second intravenous bolus of a gadolinium chelate, 0.05 mmol of gadoterate meglumine (Dotarem; Laboratoire Guerbet, Aulnay-sous-bois, France) per kilogram of body weight, was injected at a rate of 4 mL/sec and followed by a 20-mL flush of saline solution injected at the same rate. During this step, which lasted 50–65 seconds, the patient was asked to first maintain a breath hold (for about 25 seconds) and then begin a gentle, regular breathing pattern. The patient was then reinjected with the same amount of the gadolinium chelate at the end of the first-pass acquisition so that sufficient contrast between the normal and the diseased myocardial regions would be continued during delayed-enhancement imaging.
Five to 10 minutes after this first examination step, a second recirculation examination—the delayed-enhancement acquisition—was performed with the patient in diastole and with the same T1-weighted multishot gradient-echo echo-planar IR sequence and the following parameters: for three-dimensional acquisitions, 3.9/1.4/200–240, a 25° flip angle, a 270 x 340-mm field of view, a 192 x 256 matrix, 10 7–8-mm-thick short-axis sections, and an imaging time of 19 seconds; and for two-dimensional acquisitions, 7.1/3.1/200–240, a 20° flip angle, a 270 x 340-mm field of view, a 160 x 256 matrix, eight 10-mm-thick short-axis sections, and an imaging time of 10 seconds per section. Additional closely related T1-weighted (depending on each R-R interval) black-blood acquisitions were performed after gadolinium chelate administration in cases of normal first-pass perfusion and/or delayed-enhancement examination findings.
Image-reading Criteria
All MR images were displayed as continuous cine loops for review of segmental left ventricular first-pass perfusion contractile function abnormalities. Three experienced readers (J.P.L., with more than 10 years of experience in cardiovascular MR imaging; F.H., with 2 years of experience in cardiovascular MR imaging; and M.F., with 3 years of experience in cardiovascular MR imaging and more than 10 years of experience in cardiovascular nuclear medicine) who were blinded to the final diagnoses each performed independent qualitative interpretations during three successive sessions. Differences in interpretation among the readers, which occurred in six myocarditis cases, were resolved in an additional consensus reading. Segmental contractile dysfunction, as well as accessory findings such as pericardial effusion, was noted, when present.
On the first-pass perfusion MR images, those areas that showed distinct and persistent low enhancement, compared with the enhancement of the normal myocardium, more than 10 seconds after contrast material injection were considered to be low-enhancing regions. On the postcontrast delayed-enhancement MR images, those regions that showed distinctly high myocardial signal intensity were considered to be highly enhancing.
Findings were analyzed segment by segment. The left part of the myocardium was divided into 16 segments that encompassed all except the apex of the left ventricle (7), as in echocardiographic segmentation. A subendocardial, subepicardial, centromyocardial, or transmural location, as well as a nodular or bandlike enhancement pattern, was described for each diseased segment. A vascular distribution (of disease) was noted to be present or absent according to the location of the abnormally enhanced segments and, if present, to have one of the following patterns, with clear delineation between the involved vascular area and the remaining myocardium: anterior and/or septal for the left anterior descending artery, lateral for the left circumflex artery, and inferior for the right coronary artery. No attempt to measure the signal intensities of the normal and abnormal areas of enhancement was made.
Statistical Analyses
Data were analyzed by using a statistical computer program (Abacus Concepts program of StatView J-5.0; SAS Institute, Cary, NC). We studied the locations of the myocardial abnormalities by using the 2 test and compared the two disease groups (AMI and myocarditis) by using nonparametric tests. The numbers of involved segments in each group were analyzed by using the Mann-Whitney U test. We also performed statistical comparisons of other parameters between the patients with AMI and those with myocarditis by using the Mann-Whitney U test. The numbers of affected patients with disease in each given segment were compared by using the 2 test without adjustment for multiple tests. A multivariate model that linked the location of the segment and the disease status was performed.
To account for correlations between measurements obtained in the same patient, we performed binomial generalized estimating equation analysis by using the GENMOD (generalized linear models) procedure (SAS/STAT, version 8.2; SAS Institute). In a second step, the same binomial generalized estimating equation analysis of the three vascular areas was performed with a Poisson distribution; for this purpose, the left anterior descending artery area corresponded to myocardial segments 1, 2, 7, 8, 13, and 14; the right coronary artery area, to segments 3, 4, 9, 10, and 15; and the left circumflex artery area, to segments 5, 6, 11, 12, and 16. Quantitative variables are presented as means ± standard errors of the mean. P < .05 was considered to indicate significance.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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First-Pass Perfusion MR Imaging
The first-pass perfusion MR imaging findings were normal in 23 (96%) of the 24 patients with myocarditis, whereas all 31 (100%) patients with AMI had a segmental distribution of subendocardial defects (P < .001) at first-pass perfusion imaging (Figs 1,2). These data are summarized in Table 2.
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Among those patients in whom the MR imaging abnormalities did not involve the entire thickness of the myocardium (n = 33), those with myocarditis (n = 19 [79%]) more frequently demonstrated subepicardial, centromyocardial, or combined subepicardial and centromyocardial enhancement, whereas those with AMI (n = 12 [39%]) more frequently demonstrated subendocardial enhancement (P < .001). A total of 24 patients had either delayed normal enhancement (one patient in the myocarditis group vs three patients in the AMI group, nonsignificant difference) or transmural high enhancement (four patients in the myocarditis group vs 16 patients in the AMI group) (P = .01). The patients with myocarditis and delayed normal enhancement displayed nodular gadolinium-induced enhancement at additionally performed black-blood T1-weighted MR imaging.
Univariate analyses revealed that involvement of myocardial segments 5, 7, and 11 was the most significant parameter for differentiating between the two diseases (P < .05), but type 3 generalized estimating equation analysis revealed a nonsignificant correlation (P = .06). When vascular areas were considered, univariate analyses revealed that involvement of the left circumflex artery area was the most discriminant parameter (P < .001), whereas generalized estimating equation analysis revealed a significantly different repartition of the involved segments within the three vascular areas (P = .002).
Morphologic Patterns of Delayed Enhancement
The enhancement patterns of the involved myocardial regions differed between the two disease groups: A highly enhancing band was seen in all of the patients with AMI, whereas highly enhancing nodules were seen in 20 (83%) of the patients with myocarditis (P < .001). Finally, 31 (100%), 12 (39%), and 31 (100%) patients with AMI had, respectively, first-pass segmental hypoperfusion, delayed subendocardial high enhancement in a segmental vascular distribution, or a highly enhancing band pattern at presentation. Conversely, 23 (96%), 19 (79%), and 20 (83%) patients with myocarditis had, respectively, normal first-pass perfusion imaging findings, nonsubendocardial delayed high enhancement, or highly enhancing nodules at presentation.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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The present study results show that several MR imaging patterns may help to distinguish acute myocarditis from AMI—on both first-pass perfusion images and delayed-enhancement images. Myocarditis is characterized by nodular delayed enhancement in a diffuse, predominantly inferolateral subepicardial location in nonvascular territories; AMI is associated with early subendocardial perfusion defects and subendocardial or transmural delayed enhancement of a smaller number of segments, all in a vascular distribution.
Four patients with myocarditis had an isolated Q wave at ECG, abnormal coronary angiographic findings (60% right coronary artery stenosis), an early first-pass segmental defect, or a pseudosegmental vascular distribution at delayed-enhancement MR imaging. A formal diagnosis of AMI could not be established and finally was ruled out in all of these patients. Hence, all of the MR imaging sequences usually performed to diagnose myocardial infarction are useful for differentiating AMI from myocarditis.
The progression of acute myocarditis is primarily focal initially; the disease then progresses to become diffuse in approximately 10 days. The reported histologic findings of acute myocarditis are consistent with our results: The disease first manifests as interstitial edema and lymphocyte infiltration with myocyte necrosis (12).
In myocardial infarction, regional contrast enhancement occurs in a segmental vascular distribution secondary to transient (reperfused) or definitive coronary artery occlusion. Early and late enhancement may be altered by increased tissue water content due to edema, subsequent capillary compression, and impaired microvascular circulation and by inflammatory tissue (13). The area injured by prolonged ischemia is composed primarily of nonviable myocardial tissue in which myocyte death occurs first and is sometimes followed by necrosis of the endothelial cells that line the intramyocardial capillaries (14).
The homogeneous first-pass enhancement pattern in myocarditis is related to normal coronary artery blood flow within the area of inflammation, whereas in the early phase of AMI, the subendocardial defect is due to the no reflow phenomenon in tissue—as evidenced previously with contrast echocardiography or isotopic procedures—which may be observed in 30%–50% of patients with completely patent infarcted arteries (TIMI grade 3 flow) (10,14–17).
With myocarditis, the focal abnormal delayed enhancement is often subtle. During the early phase, the area of inflammation is limited, with scattered cellular damage and probably a small amount of perilesional edema (18). With AMI, the delayed enhancement is segmental, with the infarcted area appearing bright because of delayed washout. However, the delayed-enhancement MR imaging sequence has important limitations: Because gadolinium is a nonspecific element, high enhancement can be observed in several other conditions, such as increased distribution volume, microcirculatory destruction or sideration, and/or reperfusion edema.
In the patients with myocarditis in our study, the myocardial abnormalities were mainly in subepicardial locations. These data have been reported previously, with left ventricular biopsy as the reference standard (18). The subepicardial location of these anomalies may have been the consequence of increased inflammation in the most richly vascularized layers. The subendocardial or transmural location of the abnormalities in the patients with AMI was due to the course of the coronary arteries—from the epicardium to the endocardium, where they are terminal branches without collateral circulation.
The predominance of lateral and apical involvement in myocarditis has already been described (18) but without a clear explanation. In AMI, the location of disease involvement depends on the culprit coronary artery. A majority of myocardial infarctions are secondary to a diseased left anterior descending or right coronary artery, so the infarct location is mainly anterior or inferior.
Our study had some limitations. The patient selection process accounted for the disproportionately high prevalence of myocarditis in the examined population; however, this factor in no way reflects the prevalence of myocarditis among patients who present with acute coronary syndrome.
There was no reference standard for the diagnosis of myocarditis, so the final diagnosis of this abnormality was based on the discordance between increased troponin levels and the negative results of extensive coronary work-up despite the absence of provocative testing during coronary angiography: Coronary artery vasospasm was not induced by using ergonovine in the cases of normal coronary angiographic findings. We believed that performing endomyocardial biopsy would be unethical in those patients in whom a diagnosis of AMI was evident, as well as in those patients suspected of having myocarditis, owing to the reasons outlined earlier and given the limitations and risks associated with the procedure and the generally benign course of myocarditis. However, one study revealed that when the endomyocardial biopsy sample was obtained from the region of high contrast enhancement, the diagnostic yield was as high as 90% compared with a diagnostic yield of 9% when the sample was taken from a nonenhancing region (8). The myocarditis group included patients with myocarditis that mimicked AMI, none of whom presented with severe heart failure or shock, and the conditions that they had may not necessarily reflect more severe, life-threatening forms of myocarditis.
The patients with myocarditis were younger and had fewer cardiovascular risk factors than did the patients with AMI; however, these characteristics do not constitute a true selection bias. They do, however, reflect the true clinical presentation of patients with myocarditis, who are nevertheless still referred for coronary angiography in the clinical setting described in our study. The patients with myocarditis had a nonsignificant tendency to have enhancement abnormalities in more segments than the patients with AMI. The extent of anomalies and the rare vascular distribution patterns in the myocarditis group were in part secondary to a referral bias that was due to the inclusion of patients who presented with myocarditis that mimicked AMI. Moreover, because of the lower degree of contrast between the normal and the diseased myocardium in the patients with myocarditis, several segments that were affected by myocarditis may have been overlooked and thus depicted as normal.
Because of limitations that prevented the true quantification of myocardial perfusion, we did not study the quantitative relationship between MR imaging signal intensity and gadolinium chelate concentration in the region of interest.
MR imaging, with its growing value in the investigation of cardiac diseases, should gain an important role in the differential diagnosis of myocarditis or AMI, particularly in cases of normal coronary angiographic findings.
The association of a normal first-pass perfusion imaging result, nonsubendocardial delayed enhancement, and visualization of hyperenhancing nodules increases the specificity for the diagnosis of myocarditis. Furthermore, all of these features may be helpful in making the appropriate diagnosis noninvasively with MR imaging and thus precluding the use of coronary angiography in the setting of a strong presumption of acute myocarditis.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Abbreviations: AMI = acute myocardial infarction • ECG = electrocardiography • IR = inversion recovery
Authors stated no financial relationship to disclose.
Author contributions: Guarantors of integrity of entire study, J.P.L., M.F.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; approval of final version of submitted manuscript, all authors; literature research, J.P.L., F.H., E.S.; clinical studies, J.P.L., F.H., M.F.; statistical analysis, J.P.L., L.J.F., P.G.S.; and manuscript editing, J.P.L., L.J.F.
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References |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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