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Comparison of Acceleration Algorithms in Whole-Heart Four
027 T2 mapping in acute and recovered myocarditis: potential role in clinical surveillance
  1. AS Lota,
  2. R Wassall,
  3. AD Scott,
  4. PD Gatehouse,
  5. R Wage,
  6. G Smith,
  7. U Tayal,
  8. BP Halliday,
  9. JS Ware,
  10. D Firmin,
  11. SA Cook,
  12. JG Cleland,
  13. DJ Pennell,
  14. SK Prasad.
  1. Cardiovascular Biomedical Research Unit, Royal Brompton Hospital, London, UK


Background Acute myocarditis (AM) remains a challenging diagnosis with poorly defined markers of chronic active disease and/or progression to dilated cardiomyopathy. T2 mapping allows quantitative assessment of low- level myocardial oedema1 but requires further clinical evaluation alongside conventional biomarkers (troponin and BNP) prior to large-scale application.2

Aim To prospectively evaluate the role of T2 mapping in the clinical surveillance of acute myocarditis.

Methods T2 mapping was performed using T2-prepared balanced steady-state free-single shot-images on a 3 Tesla system (Skyra, Siemens) in the following patient groups:

  • Prospective patients with AM defined by clinical presentation and 2 out of 3 Lake Louise Criteria (n=11, mean age 34±10 years, all male) scanned at baseline and 3 months.

  • Retrospective patients with a history of AM (n=12, mean age 35±13 years, all male) scanned 5.7±3.9 years from acute presentation.

  • Healthy volunteers (n=9, mean age 27±6 years, 56% male).

Troponin-I and BNP were measured at the time of CMR in all patients. A global region of interest was manually drawn by a single blinded observer in the basal short-axis slice (see figure 1).

Abstract 027 Figure 1

T2-STIR and T2 mapping at the basal short-axis level in a patient with acute myocarditis affecting the lateral wall. The late gadolinium enhancement image is provided for reference.

Results In patients with acute myocarditis, mean global T2 was 42±1.4 msec compared to 40±1.3 msec in healthy volunteers (p<0.005). No difference was found between T2 values at presentation and 3 month follow-up (p=0.1), although the range of T2 values was greater at 3 months (see figure 2). In the retrospective group, mean T2 normalised to 40±1.5 msec with preserved ventricular function, comparable to healthy volunteers. Troponin normalised at follow-up in all patients, whereas BNP remained elevated in 3 patients (mean 23 ng/mL).

Abstract 027 Figure 2

Boxplot showing distribution of CMR T2 mapping values at different stages of acute myocarditis compared with healthy volunteers. The centreline in each box represents the median, whereas the lower and upper limits of each box represent the 25th and 75th percentiles, respectively. Whiskers extend to the most extreme observations.

Conclusion Our findings suggest that T2 values remain persistently elevated at 3 months following acute presentation despite normalisation of cardiac troponin levels. Increased variability in T2 values at 3 months is likely to have arisen from heterogeneity in tissue changes, unlikely to be reflected by standard AHA segments. Statistical tools such as mean absolute standard deviation (madSD)3 may improve the potential benefit of T2 mapping beyond single T2 cut-off values in this small but important subsets of patients.


  1. . Lurz P, Luecke C, Eitel I, et al. Comprehensive Cardiac Magnetic Resonance Imaging in Patients With Suspected Myocarditis: The MyoRacer-Trial. J Am Coll Cardiol2016;67(15):1800–11.

  2. . Heymans S, Eriksson U, Lehtonen J, et al. The Quest for New Approaches in Myocarditis and Inflammatory Cardiomyopathy. J Am Coll Cardiol2016;68(21):2348–64.

  3. . Baeßler B, Schaarschmidt F, Dick A,et al. Mapping tissue inhomogeneity in acute myocarditis: a novel analytical approach to quantitative myocardial oedema imaging by T2-mapping. J Cardiov Magn Reson2015;17(1):115.

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