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Original Research |
1 Department of Diagnostic Imaging, Sheba Medical Center, Tel Hashomer, 52621
Tel Aviv, Israel.
2 The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
3 Heart Institute, Chaim Sheba Medical Center, Tel Aviv, Israel.
4 Department of Emergency Medicine, Chaim Sheba Medical Center, Tel Aviv,
Israel.
Received May 22, 2008;
accepted after revision August 5, 2008.
Address correspondence to O. Goitein
(orly.goitein{at}sheba.health.gov.il).
Abstract
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MATERIALS AND METHODS. Thirty-two sequential patients (all male; average age, 33 years) with clinically suspected myocarditis were included. All patients underwent cardiac MRI with sequences dedicated for the evaluation of myocardial delayed enhancement and TTE for the evaluation of wall motion abnormalities (WMAs). Nine patients were excluded because of diagnosis of acute myocardial infarction (n = 2) or inadequate cardiac MRI technique (n = 7). Retrospective analysis of the images of the remaining 23 patients was performed.
RESULTS. An epicardial pattern of abnormal patchy myocardial delayed enhancement was seen on cardiac MRI in 21 of 23 (91%) patients. WMAs were seen on TTE in eight of 23 (35%) patients. Regional rather than global involvement was seen mainly in the inferolateral segments, with a predominance in the midventricular portion.
CONCLUSION. Cardiac MRI might have a greater impact than TTE in confirming the presence of acute myocarditis and evaluating the extent of myocardial involvement. Cardiac MRI provides noninvasive imaging that may obviate invasive procedures such as coronary catheter angiography or endomyocardial biopsy.
Keywords: cardiac MRI • myocarditis • transthoracic echocardiography
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Being universally available, transthoracic echocardiography (TTE) is the most frequently used noninvasive technique for evaluating patients with suspected myocarditis. The most common echocardiographic findings in patients with acute myocarditis are localized wall motion abnormalities (WMAs) including areas of hypokinesia, akinesia, and dyskinesia [10, 11]. These nonspecific changes cannot be used to clearly differentiate acute myocardial infarction from myocarditis.
Cardiac MRI with myocardial delayed enhancement sequences has been suggested as a noninvasive alternative for diagnosing myocarditis [12-14]. The most typical finding is epicardial delayed enhancement sparing the subendocardium, as seen in non segmental distribution [12, 13, 15-18].
The aim of this study was to correlate TTE findings with cardiac MRI findings in a cohort of patients with a high clinical suspicion for acute myocarditis.
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Myocardial delayed enhancement images were technically suboptimal in seven patients; therefore, those cases were excluded from further analysis. In two patients, cardiac MRI showed a subendocardial pattern with an adjacent hypointense rim; this finding is consistent with microvascular obstruction, a characteristic of myocardial infarction. Coronary angiography confirmed the evidence of significant coronary artery disease in both cases; therefore, these patients were excluded from the study.
Of the remaining 23 patients, 11 (48%) underwent coronary CT angiography, and three additional patients (13%) underwent invasive coronary angiography. No evidence of significant coronary artery disease (i.e., luminal stenosis > 50%) was detected in all 14 patients.
Cardiac MRI was performed using a 1.5-T scanner (Signa Excite, GE Healthcare) with a dedicated 8-channel cardiac phased-array coil. The following protocol was applied in all patients: Functional evaluation of the left ventricle (LV) was performed using a steady-state free precession in the short-axis oblique plane. The imaging parameters were TR/TE, 1.3/3.2; flip angle, 45°; bandwidth, 100 kHz; field of view, 30 cm; matrix, 128 x 256; and slice width, 6 mm. Functional analysis was performed using standard software (Mass Analysis, Advantage workstation).
Images for evaluation of myocardial delayed enhancement were obtained 10-20 minutes after IV administration of gadolinium (0.2 mmol/kg; gadoterate dimeglumine [Dotarem, Guerbet, Aulnay-sous-bois]). A T1-weighted 2D gradientecho inversion recovery sequence prepared with an inversion time of 150-300 milliseconds was adjusted for each patient to null the myocardium. The scanning parameters were 6.8/3.2; field of view, 36 x 32.4 cm; slice width, 10 mm; matrix, 256 x 224; 2 signal averages; and bandwidth, 31.3 kHz.
Myocardial delayed enhancement assessment scoring was graded according to the standardized myocardial segmentation established by the American Heart Association (AHA), with segment 17 evaluated in the vertical long axis [19]. The pattern of myocardial delayed enhancement (subendocardial, subepicardial, midmyocardial, transmural) and the percentage of LV wall involvement (0, no myocardial delayed enhancement; 1, myocardial delayed enhancement 0-25% of LV wall thickness; 2, myocardial delayed enhancement 26-50% of LV wall thickness; 3, myocardial delayed enhancement 51-75% of LV wall thickness; 4, myocardial delayed enhancement 76-100% of LV wall thickness) were assigned for each segment. The myocardial delayed enhancement score was calculated for each patient as the sum of the scores for the segments.
The TTE protocol included echocardiographic examinations performed in the left lateral position using a commercially available machine (Vivid 7, GE Healthcare; or Sonos 7500, Philips Health care). WMAs were assessed using the AHA standardized myocardial segmentation model [19]. A standard clinical scale (1, normal segment; 2, hypokinetic segment; 3, akinetic segment; 4, dyskinetic segment) was used. A WMA score was calculated for each patient as the sum of all segment scores.
The correlation between WMAs on TTE and myocardial delayed enhancement on cardiac MRI was assessed using the exact McNemar test. The correlation between myocardial delayed enhancement and WMA scores and blood troponin levels and ECG changes was analyzed using Pearson's correlation coefficient.
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Interpretable admission ECG tracings were available in 21 of the 23
patients, 17 of whom had ST-segment elevation of 
1 mm in two or more
consecutive leads; the average ST elevation sum was 5.6 ± 5 mm.
Inverted T waves were seen in two or more leads in two of four other patients
who had no suggestive ST-segment deviation. A PR-segment depression of
0.5 mm was seen in four patients, all of whom also had ST-segment elevation in
inferior leads (II, III, aVF).
Cardiac MRI showed regional rather than global involvement. Inferolateral myocardial delayed enhancement, depicted pre dominantly in the midventricular portion rather than the basal and apical portions, was seen. Epicardial delayed enhancement was present in 21 patients (91%) (Figs. 1A, 1B, 1C, 2A, 2B, and 2C), whereas TTE showed regional WMAs in only eight patients (35%) (p < 0.001). As shown in Figures 3 and 4, myocardial delayed enhancement on cardiac MRI was noted most frequently in the inferior segments (segments 4 and 10) and inferolateral segments (segments 5 and 11).
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The distribution of WMAs on TTE matched the distribution of myocardial delayed enhancement on cardiac MRI in six of the eight patients in whom WMAs were seen on TTE (Fig. 3). Thus, when present, WMAs seen on TTE most often involved the inferior and inferolateral segments at the mid LV and involved the basal and apical levels to a lesser extent.
No correlation between patient-specific myocardial delayed enhancement and WMA scores was seen.
No correlation was found between the levels of cardiac markers (i.e., troponin, CPK, and CPK-MB) and the degree of myocardial involvement seen on cardiac MRI and TTE. The average ejection fraction was 56% (range, 42-71%) and 57% (range, 40-65%) on cardiac MRI and TTE, respectively.
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WMAs on TTE were seen in eight patients: In six patients, WMAs matched the distribution of segmental myocardial delayed enhancement on cardiac MRI, and in two patients the segmental distribution of WMAs did not match the segmental distribution of myocardial delayed enhancement. Such discrepancies have also been described in previous studies [18, 20]. The typical subepicardial localization of myocardial damage in patients with myocarditis could explain the disagreement between WMAs seen on TTE and myocardial delayed enhancement seen on MRI since the endocardial layer, which is mostly responsible for the overall systolic thickening, is spared. These two techniques assess different aspects of cardiac injury in myocarditis: Cardiac MRI is capable of depicting subtle, patchy myocardial involvement, whereas TTE is a cruder technique that shows the subsequent functional injury.
Focal inflammation, cell necrosis, and tissue edema have all been implicated as being responsible for the changes seen mainly in the acute phase of myocarditis [21]. Echo cardiographic differentiation between acute myocardial infarction and myocarditis is based on the segmental distribution of WMAs, a frequently misleading criterion. Di Bella et al. [22] have recently reported a case of myocarditis in which strain Doppler imaging showed longitudinal strain abnormalities and reductions in peak systolic shortening that matched the edema seen on cardiac MRI. This longitudinal myocardial dysfunction might be related to the edema in acute myocarditis. Such developments in echo cardiography could help in the diagnosis of acute myocarditis.
Because of its excellent spatial resolution, cardiac MRI using myocardial delayed enhancement sequences can clearly show if the affected myocardium is predominantly epicardial or endocardial in location and whether the myocardial delayed enhancement pattern is consistent with a specific coronary vascular territory. Thus, cardiac MRI myocardial delayed enhancement facilitates reliable differentiation between myocarditis and acute myocardial infarction. Indeed, our study included two patients with clinically suspected myocarditis in whom myocardial delayed enhancement cardiac MRI showed clear evidence of acute myocardial infarction.
No correlation was found between the degree or extent of imaging findings on TTE and cardiac MRI and the biochemical markers of myocardial damage (i.e., troponin, CPK, and CPK-MB levels) as well as the presence and extent of ECG changes (i.e., PR-segment depression, ST elevation). These findings emphasize the lack of diagnostic accuracy of these markers for assessing myocardial damage. This finding is consistent with data previously reported by Yelgec et al. [18].
There are several limitations to our study. We did not obtain tissue samples from our patients to correlate with imaging studies. Such invasive measures are not routinely performed in our medical center and were deemed unnecessary in evaluating this patient cohort. A further limitation is the small sample size of our study. The myocardial delayed enhancement studies that were suboptimal (seven of 32) were obtained mainly at the beginning of our study, and the suboptimal quality was related to the learning curve and scanning technique. Cardiac MRI examinations in this study included steady-state free-precession sequences for function analysis and myocardial delayed enhancement sequences for gadolinium enhancement evaluation. Additional sequences (i.e., T2- and T1-weighted sequences) have been described by several groups of authors as useful in the diagnosis of myocarditis—namely, in improving the sensitivity and specificity [23, 24]. These sequences were not included in the current study.
We conclude that cardiac MRI provides noninvasive imaging that may obviate invasive procedures such as coronary catheter angiography or endomyocardial biopsy. Further studies are required to develop and maximize the information gleaned from this potent imaging technique.
Acknowledgments
Shlomi Matetzky contributed equally to this article.
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