To the editor

We read with interest the article by Tymińska et al1 published in the previous issue of Polish Archives of Internal Medicine (Pol Arch Intern Med). The authors should be congratulated on this comprehensive review. In an elegant way, they presented the etiology, pathogenesis, clinical presentation, diagnostic process, and treatment of myocarditis. However, there is an issue that needs to be raised. The authors wrote that “Gadolinium accumulates in the extracellular space where it increases the T1 signal, allowing detection of edema in myocardial tissue.” While both early enhancement (a sign of hyperemia and capillary leak) and late enhancement (a sign of necrosis and fibrosis) require administration of a gadolinium-based contrast agent, the detection of edema on T2-weighted images does not. T2-weigthed imaging as well as its quantitative counterpart, T2 mapping, are performed prior to intravenous administration of the contrast agent. It should be underlined that the presence of myocardial edema in the absence of late gadolinium enhancement represents reversible myocardial injury.2 Conversely, increased signal on postcontrast T1-weighted late gadolinium enhancement sequences demonstrates irreversible processes.3,4 Proper use of the capabilities of cardiac magnetic resonance (CMR) imaging enables the diagnosis of clinically suspected myocarditis with high sensitivity and specificity.5 Emphasis should be put on the fact that CMR is a noninvasive assessment modality as opposed to the gold standard diagnostic method—endomyocardial biopsy. Cardiac magnetic resonance is widely used in clinical practice for differential diagnosis in patients with suspected myocarditis.5 It is strongly recommended (European Society of Cardiology guidelines) for patients with myocardial infarction with nonobstructive coronary arteries. We believe that the new emerging techniques, including T1 and T2 mapping, together with extracellular volume measurements will increase the reliability of CMR in the diagnosis of myocarditis, allowing to obviate endomyocardial biopsy in the majority of clinically stable patients.