Rapid Fire Abstracts
Jenny Castaings, MSc, BMSc
Biomedical scientist
Karolinska Institutet, Sweden
Jenny Castaings, MSc, BMSc
Biomedical scientist
Karolinska Institutet, Sweden
Marcus Carlsson, MD, PhD
Professor
Lund University and Skåne University Hospital, Lund, Sweden, Sweden
Peder Sörensson, MD, PhD
Associate professor
Karolinska Institute, Sweden
Jannike Nickander, MD, PhD
MD, PhD
Karolinska Institutet, Sweden
Cardiovascular magnetic resonance (CMR) imaging with late gadolinium enhancement (LGE) plays a central role in the diagnosis of myocarditis. According to the Lake Louise consensus criteria 2018 (LLC) for myocarditis, a positive finding from either a T1 or T2 sequence represents possible myocarditis and both positive T1 and T2 for a probable myocarditis diagnosis. In clinical practice a common question is whether a non-ischemic LGE finding represents acute and chronic myocarditis. Therefore, the aim of this study was to compare the utility of native T1 and T2 mapping in patients with acute vs. chronic myocarditis.
Methods:
Consecutive patients (n=181) with a CMR diagnosis of myocarditis from December 2019 to November 2023 were retrospectively enrolled. Examinations were performed on a 1.5T or a 3T scanner (MAGNETOM Aera, MAGNETOM Sola or MAGNETOM Skyra 3T, Siemens Healthineers, Forchheim, Germany). Native T1 maps were acquired using a modified Look-Locker inversion recovery research sequence, native T2 maps using a T2 prepared steady state free precession Myomaps sequence and LGE using a free breathing phase-sensitive inversion recovery sequence. Native T1 and T2 were measured in the segments with positive LGE. Patients with a CMR consistent with sarcoidosis, dilated- or hypertrophic cardiomyopathy, were excluded, resulting in 164 patients. The cohort was divided into three subgroups, depending on the etiology; viral, caused by oncological treatment and by covid-19 or covid-19 vaccination. Further, the cohort was divided into acute, respectively chronic depending on the clinical presentation (n=143), defined by number of days from onset symptom (≤30 days=acute). If that data was not available, patients were classified according to troponin T levels with a cut-off at 50ng/L. Troponin T was collected ±10 days from the CMR. The upper limit of normal for T1 and T2 values were obtained from prior studies at our institution in healthy controls; 1087 ms for T1 and 54 ms for T2 at 1.5T and correspondingly 1342 ms and 50 ms at 3T.
Results:
All patients had positive LGE, fulfilling the T1 criteria. In acute presentation T2 mapping was negative in 26% of patients and in chronic presentation positive in 28%, Table 1. There was a high correlation between native T1 and T2 mapping at 1.5T (R2=0.64). However, when quantifying the agreement with Cohens kappa the result showed slight to fair agreement (kappa 0.2-0.3). There was no difference in native T1(p=0.461) and T2 values (p=0.821) across the different etiologies.
Conclusion:
Native T2 mapping to discriminate acute from chronic myocarditis has moderately high diagnostic utility and therefore the clinical context is important when interpreting the native T2 values in LGE positive myocarditis. Although, there is a good correlation between native T1 and T2 mapping, the concordance was poor. This may be due to native T1 being affected by both fibrosis and edema and there may be a slower reduction in native T1 values after the acute event.
The authors would like to ackowledge Kelvin Chow at Siemens Medical Solutions USA, Inc., Chicago, IL, United States, for providing the prototype sequence for T1 mapping.