Performance of t1 and t2 mapping cardiovascular magnetic resonance to detect active myocarditis in patients with recent-onset heart failure

  • BACKGROUND: This study evaluated the performance of novel quantitative T1 and T2 mapping cardiovascular magnetic resonance (CMR) techniques to identify active myocarditis in patients with recent-onset heart failure.

    METHODS AND RESULTS: Thirty-one consecutive patients with recent-onset heart failure, reduced left ventricular function and clinically suspected myocarditis underwent endomyocardial biopsy and CMR at 1.5 Tesla. The CMR protocol included standard Lake-Louise parameters as well as T1 mapping using a modified Look-Locker inversion recovery sequence and T2 mapping using a hybrid gradient and spin-echo sequence. Short-axis maps were generated using an OsiriX plug-in to calculate global myocardial T1, T2, and extracellular volume fraction. Active myocarditis was defined by ongoing inflammation on endomyocardial biopsy. Endomyocardial biopsy revealed active myocarditis in 16 (52%) of 31 patients. Neither clinical characteristics, standard Lake-Louise CMR parameters, global myocardial T1 nor extracellular volume fraction differed significantly between patients with and without active myocarditis. However, median global myocardial T2 was significantly higher in patients with active myocarditis (65 ms [Q1-Q3, 61-70 ms]) than in patients without active myocarditis (59 ms [Q1-Q3, 55-64 ms]; P<0.01). A cutoff value for global myocardial T2 of ≥60 ms provided a sensitivity, specificity, accuracy, negative and positive predictive value of 94% (70%-100%), 60% (32%-84%), 77% (60%-89%), 90% (56%-100%), and 71% (48%-89%) for active myocarditis, respectively.

    CONCLUSIONS: T2 mapping seems to be superior when compared with standard CMR parameters, global myocardial T1, and extracellular volume fraction values for assessing the activity of myocarditis in patients with recent-onset heart failure and reduced left ventricular function.

  • info:eu-repo/semantics/restrictedAccess
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