Clinical application and technical considerations of T1 & T2(*) mapping in cardiac, liver, and renal imaging

Abstract

Pathological tissue alterations due to disease processes such as fibrosis, edema and infiltrative disease can be non-invasively visualized and quantified by MRI using T₁ and T₂ relaxation properties. Pixel-wise mapping of T₁ and T₂ image sequences enable direct quantification of T₁, T₂(*), and extracellular volume values of the target organ of interest. Tissue characterization based on T₁ and T₂(*) mapping is currently making the transition from a research tool to a clinical modality, as clinical usefulness has been established for several diseases such as myocarditis, amyloidosis, Anderson-Fabry and iron deposition. Other potential clinical applications besides the heart include, quantification of steatosis, cirrhosis, hepatic siderosis and renal fibrosis. Here, we provide an overview of potential clinical applications of T₁ andT₂(*) mapping for imaging of cardiac, liver and renal disease. Furthermore, we give an overview of important technical considerations necessary for clinical implementation of quantitative parametric imaging, involving data acquisition, data analysis, quality assessment, and interpretation. In order to achieve clinical implementation of these techniques, standardization of T₁ and T₂(*) mapping methodology and validation of impact on clinical decision making is needed.

Figure 1.

Magnetization inversion recovery for T₁, T₂and T₂* mapping. T1 recovery curve showing increase in the longitudinal magnetization with longer inversion times due to T₁ recovery, left curve (A). Different images are obtained following an inversion pulse at multiple different inversion times for T₁ mapping during the same phase of the cardiac cycle in subsequent heart beats (B). T₂ and T₂* recovery curves showing that as the TE increases, the myocardial signal intensity decreases due to T₂ decay, (long curve), and due to static field inhomogeneities for T₂* decay (short curve) (C). Different gradient echo images are acquired at different echo times for T₂* mapping (D), and different spin-based preparation images are acquired at different echo times for T₂ mapping (E).

Figure 2.

Calculation of ECV. Calculation of ECV using the inverse of the signal in each pixel (1/T₁) is used to generate an R₁ map (F). The ΔR₁ map of the blood pool (ΔR₁blood) and myocardium (ΔR₁ myocard) is generated by subtracting the corresponding precontrast R₁ map from the post-contrast R₁ map. ΔR₁ map pixel values are multiplied by one minus the hematocrit level, and then divided by the mean ΔR₁blood in order to calculate ECV. The final result is a colour encoded parametric map displaying the pixel-by-pixel ECV values. ECV, extra cellular volume.

Figure 3.

Example of correspondence of ECV and LGE in a patient with PVCs with focal fibrosis. LGE shows some enhancement basal septal, which is confirmed by the ECV map constructed using the pre- and post-contrast T₁ maps. The ECV in the region of interest was 45% localized in focal septal hypertrophy, which is the likely origin of the PVC's. Quantitative T₁ and ECV maps were automatically reconstructed on a voxel-by-voxel basis after data acquisition using the T₁ map processing tool (Medis Research Edition, v. 3.0, Leiden). ECV, extra cellular volume; LGE, late gadolinium enhancement; PCV, premature ventricular contraction.

Figure 4.

Example of added value of ECV compared to LGE in a patient with familial hypertrophic cardiomyopathy with diffuse fibrosis. Non-dilated left ventricle with septal hypertrophy with diffuse fibrosis [serum hematocrit of 45%, native T₁ septum 1315 ms (N < 1350 ms), and ECV 42% (N < 35%)]. Quantitative T₁ and ECV maps were automatically reconstructed on a voxel-by-voxel basis after data acquisition using the T₁ map processing tool (Medis Research , v. 3.0, Leiden). ECV, extra cellular volume; LGE, late gadolinium enhancement.

Figure 5.

Tissue characterization using native T₁ and ECV fraction. Absolute values for native T₁ depend greatly on field strength (1.5 or 3 T), pulse sequence (MOLLI or ShMOLLI), scanner manufacturer and post-processing. For the purpose of comparability, only studies using 1.5 T scanners were considered in this figure. Reprinted from Haaf et al publisher BioMed Central under the terms of the Creative Commons Licence. ECV, extra cellular volume; MOLLI, modified look-locker imaging; ShMOLLI, shortened MOLLI.

Figure 6.

T₂* mapping of heart (left) and liver (right) in a childhood cancer survivor at risk of secondary hemosiderosis after multiple blood transfusions and chemotherapy for acute lymphatic leukemia. Parametric imaging of heart and liver using StarQuant (Philips) heart and LiverMultiScan (Perspectum). The myocardial T₂* value was 38 ms (normal reference > 20 ms), and liver T₂* value was 13.3 ms, indicating normal T₂* values of the heart and minimal iron deposition in the liver. Quantitative T₂ maps were automatically reconstructed on a voxel-by-voxel basis after data acquisition using the T₂ map processing tool (Medis Research Edition, v. 3.0, Leiden).

Figure 7.

Typical appearance of T₁, ECV, T₂, and T₂* maps in heart, liver, and kidney of healthy subjects (upper row) and in patients with myocardial and liver disease (second to fourth row) (Medis Research Edition, v. 3.0, Leiden). Adapted by permission from BioMed Central under the terms of the Creative Commons Licence, and adapted by permission from BMJ Publishing Group Limited.ECV, extra cellular volume.