In myocarditis, inflammation within the myocardium can lead to myocyte necrosis and subsequent myocardial fibrosis. Myocarditis may be caused by many agents (viruses, bacteria, drugs, toxins, autoimmune) and presents with a wide range of symptoms from transient fatigue, acute chest pain to heart failure or sudden cardiac death [
1‐
3]. In addition, a significant proportion of dilated cardiomyopathies may be caused by unrecognized myocarditis [
4,
5]. Because of the heterogeneity of symptoms, the diagnosis of myocarditis is challenging [
6,
7]. Endomyocardial biopsy (EMB) with (immune-) histology is the gold standard for the diagnosis of myocarditis. However, EMB is an invasive method with a low sensitivity (20–75 %) [
8‐
10] due to sampling error (if the sample is taken from a non-involved area of the myocardium) [
3,
11] and with significant risk (perforation, tamponade, in 0.1–0.5 % of the patients [
12,
13]. Cardiovascular Magnetic Resonance (CMR) is increasingly used as a non-invasive diagnostic tool for patients with suspected myocarditis [
7,
14‐
17]. CMR is the non-invasive reference standard for the quantification of ventricular volumes and function. The same CMR method used for the assessment of viability in coronary artery disease (Late Gadolinium Enhancement; LGE) can be used to visualize focal lesions in myocarditis [
18]. However, conventional CMR methods aiming to assess diffuse, non-focal involvement of the myocardium suffer from large overlap between normal and disease states [
19]. Thus, a non-invasive method that allows the detection of widespread inflammation and diffuse fibrosis is needed. Cardiac T1 mapping is a parametric CMR method allowing for characterizing the myocardium by directly quantifying the signal intensity. In contrast to conventional CMR methods, T1 mapping can detect not only focal changes but also global myocardial injury without the need for an extra-cardiac reference tissue [
20‐
23]. Thus, T1 mapping is a non-invasive imaging method that may help in the diagnosis and follow-up of patients with myocarditis without the risks of invasive biopsy.
Experimental autoimmune myocarditis (EAM) is a well-known myocarditis model in rats, which mimics human myocarditis in the acute and chronic phases [
24‐
26]. The histological findings in EAM are similar to human myocarditis, with fibrosis and myocyte necrosis involving mononuclear cell infiltration [
27‐
29].
We aimed to study the changes in myocardial T1 in the course of myocarditis. Using EAM rats, we assessed the myocardium at baseline and then in the acute and chronic stages of myocarditis, and compared the results with histological and immune-histological findings.