Myocardial tissue characterization by magnetic resonance imaging: novel applications of T1 and T2 mapping

Abstract

Cardiac magnetic resonance (CMR) imaging is a well-established noninvasive imaging modality in clinical cardiology. Its unsurpassed accuracy in defining cardiac morphology and function and its ability to provide tissue characterization make it well suited for the study of patients with cardiac diseases. Late gadolinium enhancement was a major advancement in the development of tissue characterization techniques, allowing the unique ability of CMR to differentiate ischemic heart disease from nonischemic cardiomyopathies. Using T2-weighted techniques, areas of edema and inflammation can be identified in the myocardium. A new generation of myocardial mapping techniques are emerging, enabling direct quantitative assessment of myocardial tissue properties in absolute terms. This review will summarize recent developments involving T1-mapping and T2-mapping techniques and focus on the clinical applications and future potential of these evolving CMR methodologies.

FIGURE 1

T1 mapping in acute myocardial infarction. Edema T2W images (left column), acute LGE images (center), and ShMOLLI T1 mapping (right column) are displayed. Two sets of images (A and B) corresponding to 2 separate patients are shown. A, A case of transmural inferior STEMI. Both edema (T2W) and LGE depict an area of increased signal intensity; in the same region T1 mapping depicts significantly increased T1 values (shown in red) compared with the remote unaffected myocardium (normal T1 values shown in green). B, A case of subendocardial NSTEMI. Although the T2W images show only a mild increase in brightness, there is an area of increased T1 values exceeding the area of LGE enhancement. It is noteworthy that the peak troponin I level was significantly different in the 2 patients (peak troponin I 50 mg/mL in the STEMI patient vs. 7 mg/mL in the NSTEMI patient). NSTEMI indicates non-ST elevation myocardial infarction; STEMI, ST elevation myocardial infarction (modified from Dall'Armellina et al, figure 1). Adaptations are themselves works protected by copyright. So in order to publish this adaptation, authorization must be obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.

FIGURE 2

T1 mapping in acute myocarditis. A, Dark-blood T2W imaging demonstrating increased signal intensity in the mid-lateral wall (arrows). B, Bright-blood T2W imaging demonstrating increased signal intensity in the mid-lateral wall (arrows). C, Shortened MOLLI (ShMOLLI) T1 map demonstrating increased T1 values (1100 to 1200 ms) in the lateral wall (arrows). D, LGE imaging demonstrating mid-wall enhancement in the lateral wall (arrows) (modified from Ferreira et al, figure 1). Adaptations are themselves works protected by copyright. So in order to publish this adaptation, authorization must be obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.

FIGURE 3

T1-mapping in amyloidosis. CMR end-diastolic frame from cine (left panel), ShMOLLI noncontrast T1 map (middle panel), and LGE images (right panel) in a normal volunteer, a cardiac amyloid patient, and an aortic stenosis patient. Note the markedly elevated myocardial T1 time in the cardiac amyloid patient (1170 ms, into the red range of the color scale) compared with the normal control (955 ms) and the patient with aortic stenosis and left ventricular hypertrophy (998 ms). ED indicates end diastolic (modified from Karamitsos40). Adaptations are themselves works protected by copyright. So in order to publish this adaptation, authorization must be obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.

FIGURE 4

Examples illustrating excellent agreement between LGE and ECV in cases of focal abnormalities in myocardial ECV. Precontrast T1 maps (top row), postcontrast T1 maps (second row), LGE (third row), and ECV maps (bottom row) for patients with: (A) chronic MI, (B) acute myocarditis, and (C) HCM. HCM indicates hypertrophic cardiomyopathy; MI, myocardial infarction (modified from Kellman57). Adaptations are themselves works protected by copyright. So in order to publish this adaptation, authorization must be obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.

FIGURE 5

T2 maps, T2-STIR, and LGE images in patients with acute myocardial infarction. A, A 53-year-old male patient admitted with ST-segment elevation myocardial infarction (STEMI) in the circumflex artery territory. Quantitative T2 in the infarct region was 72 ms compared with 56 ms in the remote myocardium. B, A 75-year-old male patient presenting with left anterior descending artery territory STEMI. T2 of the infarct zone measured by T2 mapping was 66 ms compared with 51 ms in the remote myocardium. C, Basal short-axis slice in a 58-year-old female patient presenting with non-STEMI in the right coronary artery territory. T2 measured within the region of the infarct was 71 ms compared with 58 ms in the remote myocardium. D, A 62-year-old male patient admitted with a STEMI in the left anterior descending artery territory. Quantitative T2 of the infarcted segments was 73 ms. By T2 mapping, a rim with high signal intensity circumferential to the left ventricle is seen (*), consistent with postinfarct pericardial effusion. The region of infarct is indicated by arrowheads. STEMI indicates ST-segment elevation myocardial infarction; T2-STIR, T2W short tau inversion recovery (modified from Verhaert77). Adaptations are themselves works protected by copyright. So in order to publish this adaptation, authorization must be obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.