T2* mapping - myocardium

Last revised by Joachim Feger on 13 Apr 2024

T2* mapping is a magnetic resonance imaging technique used to calculate the T2* time of tissue and display them voxel-vice on a parametric map. It is used for myocardial tissue characterization 1-4 and has been investigated for other tissues 5,6.

T2* relaxation time has become useful in the evaluation of myocardial iron content and assessment of myocardial hemorrhage, specifically for the following indications 1-3:

Patients with transfusion-dependent anemia or hemochromatosis showing T2* values <20 ms are at risk for arrhythmia and systolic dysfunction and with T2* levels <10 are at high risk for heart failure 2,7.  In the setting of acute myocardial infarction, T2*-mapping values <20 ms indicate microvascular injury 8.

T2* mapping is usually based on gradient echo (GRE) sequences.

T2* [ms] results principally from variations in the static magnetic field throughout the tissue which will be added to random mechanisms. Thus, T2* is a time constant for the decay of transverse magnetization, but in the presence of local magnetic field inhomogeneities, it is shorter than T2 [ms] alone 1-4

T2* mapping acquisition has been recommended on a 1.5 Tesla MR scanner with a multi-gradient echo technique typically with 8 equally spaced echoes ranging from 2 ms to 18 ms 1-3.

A black-blood sequence has been recommended because of better image quality, and intra- and interobserver reproducibility 3.

Like T2 values, T2* can be calculated pixel-wise from a signal intensity versus time curve fitting model 2,3. The motion between the images needs to be corrected.

It has been recommended to assess T2* for iron overload in the interventricular septum 1-3.

A 3-tier risk model (low, intermediate and high risk) has been recommended 1-3:

  • T2* >20 ms or R2* <50 Hz

    • no iron overload

  • T2* 10-20 ms or R2* 50-100 Hz

    • mild to moderate iron overload

  • T2* <10 ms or R2* >100 Hz

    • severe iron overload

The large cardiac veins can induce artifacts due to susceptibility differences between the deoxygenated blood in the veins and the adjacent myocardium 2. This is less of a problem in black-blood sequences 2. Epicardial fat at the anterior wall and the heart-lung interface mostly apparent at the free lateral wall are other sources of artifacts 2.

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