Cardiac magnetic resonance is in the present the leading non-invasive imaging method for patients with myocarditis [24, 97, 98, 99]. It is even described by some authors as one of the basic examinations and in stable patients, it is preferred to perform CMRI earlier than EMB [24]. CMRI advantages are primarily in its ability of the structural and functional heart characteristics evaluation with higher accuracy than ECHO, and it is primarily used for the evaluation of changes of the myocardial tissue characteristics [99, 100], when it is possible to detect the myocardial oedema, myocardial hyperaemia as a result of the inflammatory process, and especially necrosis or in later phases fibrosis of the myocardium [100, 106]. Diagnosis of myocarditis is further supported by the presence of the pericardial effusion [107]. Gadolinium contrast agent is administered to the patients for the evaluation of the myocardial necrosis/fibrosis.
For the evaluation of myocardial oedema, T2 sequences are used, when the area of myocardial oedema has higher signal intensity than surrounding tissue [106]. However, there are described numerous difficulties when using this sequence, e.g. lower imaging quality, artifacts that may distort the results and that in the case of the diffuse myocardial damage, oedema does not have to be displayed sufficiently [106]. Thus, the ratio of values of the myocardial signal intensity (SI) and skeletal muscle signal intensity is used for the diagnosis of oedema. This ration is called oedema ratio (ER).
Hyperaemia is detected by T1 sequences. The principle of this CMRI part is a comparison of the myocardial SI before and immediately after the administration of a contrast agent what is then called as EGE (early gadolinium enhancement), Similar to T2 sequences, the comparison of the myocardial and skeletal muscles SI is used for the diagnosis of hyperaemia [106].
An important part of this examination is the evaluation of LGE (late gadolinium enhancement) which proves myocardial necrosis or in later phases fibrosis of the myocardium because gadolinium passes just through the membrane of damaged cardiomyocytes [106]. Most frequently, LGE is localized in the left ventricular free wall (often lateral) or in interventricular septum in subepicardial and/or midmyocardial layer [99, 100, 106], (Pic. 11). Subendocardial localization is described in ischemic myocardial damage [106]. The necrosis/fibrosis area may be a potential arrhythmogenic substrate [106].
To increase the utilization of the examination, Lake Louise Criteria have been created (Table 3) which describes besides above-mentioned procedures even possible indications and criteria for the confirmation of the diagnosis of myocarditis according to CMRI [107].
Picture 11: CMRI of a 17-year-old male with the 2nd attack of myocarditis, distinct chest pain, elevation of troponin and increasing CRP. CMRI with the presence of LGE (red arrows) in acute phase of myocarditis and 6 months later again with the presence of LGE (Department of Radiology of the 2nd Medical School and Motol Hospital, by Adla M.D.)
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Picture 13: 15-year-old male with chronic myocarditis (inflammatory infectious cardiomyopathy). Aetiology unknown, did not prove even by endomyocardial biopsy. On the MRI scan, apperant a distinctive dilatation and dysfunction of both ventricles. LV EF 21 % (norm > 55 %), RV EF 26 % (norm > 50 %). After the contrast agent administration, a strip of late enhancement is visiable in the middle and external layer of the posterior and lateral wall of the left ventricle (Department of Radiology of the 2nd Medical School and Motol Hospital, by Adla M.D.)
Video: see picture 13
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| In the setting of clinically suspected myocarditis, CMRI findings are consistent with myocardial inflammation, if at least two of the following criteria are present: |
| I. Regional or global myocardial signal intensity increase in T2-weighted edema images |
| II. Increased global EGE ratio between myocardial and skeletal muscle in T1-weighted images |
| III. There is at least one focal lesion with non-ischemic regional distribution in LGE. |
| A CMRI study is consistent with myocyte injury and/or scar caused by myocardial inflammation if Criterion 3 is present. |
| A repeat CMRI study between 1 and 2 weeks after the initial CMRI study is recommended if |
| None of the criteria are present, but the onset of symptoms has been very recent and there is strong clinical evidence for myocardial inflammation |
| One of the criteria is present |
| The presence of LV dysfunction or pericardial effusion provides additional, supportive evidence for myocarditis. |
Table 3: Lake Louise Criteria, diagnosis of myocarditis in confirmed with 67 % sensitivity and 91 % specificity when at least 2 from 3 criteria are present [107].———————————————————————————————————————————————————————————————————————————-
LGE presence is described as an indicator of worse prognosis and increased mortality risk [27]. In a German-American study [27], patients with LGE presence had generally more distinctive left ventricular impairment and higher mortality than those without LGE presence (e. g. LV EF 37,5 % x 53,0 %),
However, negative CMRI result does not exclude the diagnosis of myocarditis because according to the references the examination does not have to provide sufficient sensitivity for the detection of myocarditis in the case of minor myocardial impairment [106]. The most frequently described disadvantage of the examination is its limited availability, time demands and primarily the fact that it is not able to distinguish specific types of myocarditis (GCM etc.), it does not provide information about aetiology of the inflammation and that the performance of LGE examination alone does not distinguish acute and chronic inflammation [106].
Author of the opening picture: Department of Radiology of the 2nd Medical School and Motol Hospital, by Adla M.D.
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References:
24) CAFORIO, A.L.P, PANKUWEIT S., ARBUSTINI E., et al. Current state knowledge on aetiology, diagnosis, management, and Therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Disease. European Heart Journal. 2013, 34(-), 2636–2648.
27) GRÜN, S., SCHUMANN J. a et al. Long-Term Follow-Up of Biopsy-Proven Viral Myocarditis: Predictors of Mortality and Incomplete Recovery. JACC. 2012, 59(18), 1604-1615.
97) KUCHYNKA P. Kapitola 8.1. Akutní myokarditida. In: MOŤOVSKÁ, Z. a et al. Novinky v akutní kardiologii. Praha: Mladá fronta, 2016. pp. 292–303. ISBN 978-80-204-3903
98) KINDERMANN, I. a et al. Update on Myocarditis. Journal of the American College of Cardiology. 2012, 59(9), 779-792.
99) KUCHYNKA, P. a et al. Myokarditida a zánětlivá kardiomyopatie. Kapitoly z kardiologie. 2013, 3(-), 87-91.
100) KREJČÍ, J. Myokarditidy a zánětlivé kardiomyopatie. Kardiologická Revue Interní Medicína. 2015, 17(4), 288-294.
106) PLEVA, M. Kapitola 6: Akutní myokarditida. In: PLEVA, M. a P. OUŘEDNÍČEK. MRI srdce. Praha: Grada Publishing, 2012. pp. 83-86. ISBN 978-80-247-3931-1.
107) FRIEDRICH, M.G. a et al. Cardiovascular Magnetic Resonance in Myocarditis: A JACC White Paper. Journal of the American College of Cardiology. 2009, 53(17), 1475-1487.
