Cardiac magnetic resonance (CMR) is an imaging technique that has substantially evolved over the last 15 years to become a valuable clinical and research tool in cardiology.1,2 With the development of the late gadolinium enhancement (LGE) technique using an inversion-recovery T1-weighted (T1W) sequence in 1999, the identification of the patterns and distribution of scar and fibrosis became possible for differentiating ischemic from nonischemic cardiomyopathies.1,3,4 Similarly, the refinement of T2W techniques enabled the detection of myocardial edema and inflammation, further establishing the role of CMR in myocardial tissue characterization.5 Recently, parametric T1-mapping and T2-mapping techniques opened a new frontier for CMR to explore tissue characteristics in more quantitative terms.6,7 These novel mapping strategies offer the promise of objective assessment of myocardial tissue properties, providing an absolute quantitative measure rather than just a qualitative (visual) or semiquantitative evaluation (on the basis of comparisons of relative signals), which can be subjective and may underestimate or overestimate disease.
This review will focus on the clinical applications of T1 and T2 mapping with particular focus on recent developments in this rapidly evolving field.
MYOCARDIAL T1 AND T1 MAPPING
T1 is the longitudinal (or spin-lattice) relaxation time of a tissue. T1 mapping refers to parametric maps that are generated from a series of images acquired with different T1 weighting so that each pixel can be assigned a T1 value.7 T1 maps can be displayed using color or thresholded scales to enable quantitative visual interpretation.8,9 Each tissue type exhibits a characteristic range of normal T1 relaxation times at a particular field strength, deviation from which may be indicative of disease. Measured myocardial T1 values are also influenced by various physiological and technical factors, including temperature, disease, age, sex, heart rate, and the pulse sequence used.10–12
The Modified Look-Locker Inversion Recovery (MOLLI) method developed by Messroghli et al13 in 2004 opened a new frontier of clinical applications for myocardial T1 mapping. Newer variants, based on inversion-recovery, saturation-recovery, or hybrid approaches, continue to emerge, enabling faster acquisition times and minimizing sources of error such as heart-rate dependency, motion, off-resonance, and partial volume effects.14–20 Although MOLLI-based sequences are the most widely used and most extensively validated,11,13,20,21 the saturation-recovery single-shot acquisition sequence is a very promising novel approach demonstrating good T1 measurement accuracy in phantoms.14 This contrasts with MOLLI techniques, which are known to underestimate T1.20,22 This is attributed in part to T223 and also more recently to the presence of a physiological but MR-invisible proton pool that, although affecting the technical accuracy of MOLLI, may actually improve its sensitivity to disease.24
Myocardial T1-mapping methods are used for native (ie, without the use of gadolinium-based contrast agents) and also for postcontrast T1 measurements. In combination with hematocrit levels, these enable the quantification of extracellular volume fraction (ECV).25
Native myocardial T1 reflects a composite signal from both the intracellular (predominantly myocytes) and the extracellular compartment. Gadolinium-based contrast agents shorten T1 times, and the physiological differences in redistribution after administration directly affect tissue T1.22,26–29 However, isolated postcontrast T1 values are influenced by a number of factors, including native T1, the type and dosage of gadolinium contrast used, and the postcontrast acquisition time within the contrast pharmacodynamics redistribution process. The latter depends on numerous systemic variables, such as body fat percentage, hematocrit levels, and glomerular filtration rate.30–32 Therefore, currently preferred outputs for myocardial T1 quantification are native T1 and ECV.7
There is increasing interest in the study of the myocardial interstitium as a determinant of disease course and as a therapeutic target in a number of cardiac conditions. ECV measures the extracellular space, and, in the absence of myocardial edema or other factors that could expand the interstitial space (such as amyloid), expansion of the myocardial collagen volume fraction is responsible for most of the extracellular matrix expansion.7
ECV can act as a surrogate for (but not as a direct measure of) myocardial interstitial fibrosis.7 It is possible to quantify myocardial ECV in vivo using the equilibrium CMR technique,33 which showed good correlation with histologic collagen volume fraction.34 Equilibrium CMR assumes an equilibrium steady state between the intravascular and interstitial spaces as a strict, 2-compartment model and requires a constant infusion of contrast to achieve a steady state. This protocol may be abbreviated by using the bolus contrast technique with delayed (15 min) postcontrast measurement, known as dynamic-equilibrium CMR,32 which closely approximates the steady state and is sufficient for most myocardial ECV applications.7 ECV calculation can correct for some of the variables confounding isolated postcontrast T1 values, but its accuracy also relies on the assumption that the effect of contrast is equal in the 2 compartments, which is subject to debate.35 Additional confounders include incomplete dynamic equilibrium, contrast transfer into other compartments, and a faster renal clearance than exchange rate.31
Clinical Applications of T1 Mapping
The clinical utility of native T1 mapping relies on a normal range with small variability14,19,36 and high sensitivity to disease. Elevated T1 times in the myocardium have been reported in a number of commonly encountered cardiac conditions including myocardial infarction,9 myocarditis,37 hypertrophic and dilated cardiomyopathy (DCM),38,39 cardiac amyloidosis,40 cardiac involvement in systemic diseases,41–43 and diffuse fibrosis in patients with aortic stenosis.44
In particular, native myocardial T1 is prolonged by excess free water content,45–47 such as that due to acute edema, inflammation, or pooling within an expanded interstitial space. Ferreira et al9 demonstrated for the first time that native T1 mapping detects acute myocardial edema in patients with Tako-tsubo cardiomyopathy and regional stunning with high diagnostic accuracy compared with conventional T2W techniques. Dall’Armellina et al48 found that the diagnostic performance of T1 mapping for detecting acute myocardial injury was at least as good as that of T2W CMR in patients with ST elevation myocardial infarction and superior to T2W imaging in patients with non-ST elevation myocardial infarction (Fig. 1). For determining the area at risk after acute myocardial infarction, native T1 mapping and T2 mapping yield similar quantitative results and good agreement with microspheres in animal models.49 Recently, native T1 mapping was shown to have superior sensitivity compared with T2W and LGE techniques in detecting acute myocarditis (Fig. 2), which may be especially useful in detecting subtle focal disease and when gadolinium-based contrast imaging is not feasible.37 Furthermore, native myocardial T1 values are significantly elevated in patients with DCM and hypertrophic cardiomyopathy compared with normal controls38,50; T1 values are also increased in apparently normal regions without LGE in both conditions. These findings suggest that native T1 mapping provides information on myocardial tissue characteristics beyond that achieved by standard CMR techniques. The clinical utility of native T1 mapping was also shown in patients with cardiac amyloidosis (Fig. 3) who have significantly elevated T1 values compared with normal subjects and patients with aortic stenosis.41 Native T1 mapping may be particularly useful for identifying amyloid patients with possible or definite cardiac involvement given its high diagnostic accuracy and the difficulty in applying conventional LGE in this cohort.40 Increased native T1 values have been reported in patients with human immunodeficiency virus51 and patients with systemic lupus erythematosus and cardiac involvement.52 In patients with severe aortic stenosis, native T1 values are increased and correlate with the degree of biopsy-quantified collagen volume fraction.45 Native myocardial T1 values may be lowered by water-protein interactions and fat or iron content and thus can also serve as a diagnostic tool in characterizing Anderson-Fabry disease,10 fat in cardiac masses,53 and myocardial siderosis.54
ECV may serve as a marker for myocardial fibrosis in a number of myocardial diseases.25,31,45,55 The ECV of the normal myocardium has been reported to be in the range of 24% to 28%.21,56 ECV expansion has been demonstrated in a number of cardiac conditions including myocardial infarction, myocarditis, hypertrophic cardiomyopathy and DCM, cardiac amyloidosis, diabetes, obesity, congenital heart disease with myocardial dysfunction, and other cardiac conditions characterized by diffuse myocardial fibrosis (Fig. 4).57–65 The detection of interstitial myocardial fibrosis may allow early therapeutic intervention before irreversible changes occur.
MYOCARDIAL T2 AND T2 MAPPING
T2 (or spin-spin) relaxation time is the time constant governing the exponential decay of transverse magnetization. The fractional increase in T2 is substantially larger than the fractional increase in T1 when water content is increased, and this relationship was demonstrated in a canine model of acute myocardial infarction 30 years ago.46 Various technical improvements since then have enabled the wide clinical use of T2W CMR for the qualitative or semiquantitative detection of myocardial edema and inflammation.66,67 However, there are a few well-recognized limitations of conventional T2W techniques,5 including the need for a “normal” reference region of interest, either in remote myocardium or skeletal muscle, which can lead to false-negative results when these reference areas are also affected in systemic processes.37,68,69
Quantification of T2 myocardial relaxation times promises to circumvent these limitations and is achieved by collecting multiple images with different T2-weighting, providing multiple points along the T2 decay curve for fitting of an exponential signal decay model.6 Initial T2-mapping techniques based on dark-blood turbo spin echo sequences were sensitive to ghosting and motion artifacts.6 Recently, bright-blood T2 prep-based pulse sequences showed improved results.70 These T2-mapping techniques exhibit heart-rate dependency, sensitivity to the order of acquisition,71 and flip angle, with incomplete T1 recovery resulting in T1 weighting and errors in the T2 relaxation time measurements, although increasing the sampling interval can reduce this effect.72 Currently, normal measured T2 times exhibit larger interindividual variability compared with measured T1 times70,72,73 but nevertheless have been shown to be useful in detecting disease.
Clinical Applications of T2 Mapping
T2 mapping can detect edematous myocardial territories in a variety of cardiac pathologies, including acute myocardial infarction, myocarditis, Tako-tsubo cardiomyopathy, and heart transplant rejection.72,74–77 Verhaert et al77 assessed T2 mapping in patients with acute myocardial infarction and found that myocardial segments characterized by recent ischemic injury can be quantitatively differentiated from remote myocardium by their higher T2 value (Fig. 5). Another study from the same group showed the usefulness of T2 mapping in suspected myocarditis or Tako-tsubo cardiomyopathy, demonstrating that T2 mapping can identify myocardial involvement beyond conventional CMR techniques such as T2W and LGE imaging. T2 mapping has also been used as a noninvasive tool for cardiac transplant monitoring with promising preliminary findings in small cohorts.74
T1-mapping and T2-mapping techniques have already demonstrated clinical usefulness as quantitative tissue characterization MR techniques in a variety of common cardiac conditions. Further technical improvements are expected to advance their clinical application in the detection of acute, subacute, and subclinical pathologies. Consensus within the CMR community regarding methodological issues and standardization is needed to facilitate wider clinical utility. Multicenter studies should be performed to assess not only the diagnostic value of these techniques but also their utility in therapeutic monitoring and prognostication.
The authors acknowledge support by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre based at The Oxford University Hospitals NHS Trust and the University of Oxford. Stefan Neubauer acknowledges support from the British Heart Foundation Centre of Research Excellence, Oxford.
1. Karamitsos TD, Francis JM, Myerson S, et al..The role of cardiovascular magnetic resonance imaging in heart failure.J Am Coll Cardiol.2009;54:1407–1424.
2. Pennell DJ.Cardiovascular magnetic resonance.Circulation.2010;121:692–705.
3. Kim RJ, Fieno DS, Parrish TB, et al..Relationship of mri delayed contrast enhancement to irreversible injury, infarct age, and contractile function.Circulation.1999;100:1992–2002.
4. Karamitsos TD, Dall’Armellina E, Choudhury RP, et al..Ischemic heart disease: comprehensive evaluation by cardiovascular magnetic resonance.Am Heart J.2011;162:16–30.
5. Eitel I, Friedrich MG.T2-weighted cardiovascular magnetic resonance in acute cardiac disease.J Cardiovasc Magn Reson.2011;13:13.
6. Salerno M, Kramer CM.Advances in parametric mapping
with CMR imaging.JACC Cardiovasc Imaging.2013;6:806–822.
7. Moon JC, Messroghli DR, Kellman P, et al..Myocardial T1 mapping and extracellular volume quantification: a society for cardiovascular magnetic resonance (SCMR) and CMR working group of the european society of cardiology consensus statement.J Cardiovasc Magn Reson.2013;15:92.
8. Ferreira VM, Piechnik SK, Firoozan S, et al..Acute chest pain and massive LV hypertrophy in a 38-year-old man.Heart.2013[Epub ahead of print].
9. Ferreira V, Piechnik S, Dall’Armellina E, et al..Non-contrast T1-mapping detects acute myocardial edema
with high diagnostic accuracy:a comparison to T2-weighted cardiovascular magnetic resonance.J Cardiovasc Magn Reson.2012;14:42.
10. Sado DM, White SK, Piechnik SK, et al..Identification and assessment of anderson-fabry disease by cardiovascular magnetic resonance noncontrast myocardial T1 mapping.Circulation Cardiovasc Imaging.2013;6:392–398.
11. Messroghli DR, Plein S, Higgins DM, et al..Human myocardium: single-breath-hold mr T1 mapping with high spatial resolution—reproducibility study.Radiology.2006;238:1004–1012.
12. Bottomley PA, Foster TH, Argersinger RE, et al..A review of normal tissue hydrogen NMR relaxation times and relaxation mechanisms from 1-100 MHz: dependence on tissue type, NMR frequency, temperature, species, excision, and age.Med Phys.1984;11:425–448.
13. Messroghli DR, Radjenovic A, Kozerke S, et al..Modified look-locker inversion recovery (MOLLI) for high-resolution T 1 mapping of the heart.Magn Reson Med.2004;52:141–146.
14. Chow K, Flewitt JA, Green JD, et al..Saturation recovery single-shot acquisition (SASHA) for myocardial T1 mapping.Magn Reson Med.2013[Epub ahead of print].
15. Higgins DM, Ridgway JP, Radjenovic A, et al..T1 measurement using a short acquisition period for quantitative cardiac applications.Med Phys.2005;32:1738–1746.
16. Lee JJ, Liu S, Nacif MS, et al..Myocardial T1 and extracellular volume fraction mapping at 3 Tesla.J Cardiovasc Magn Reson.2011;13:75.
17. Schelbert E, Testa S, Meier C, et al..Myocardial extravascular extracellular volume fraction measurement by gadolinium cardiovascular magnetic resonance in humans: slow infusion versus bolus.J Cardiovasc Magn Reson.2011;13:16.
18. Xue H, Shah S, Greiser A, et al..Motion correction for myocardial T1 mapping using image registration with synthetic image estimation.Magn Reson Med.2012;67:1644–1655.
19. Piechnik S, Ferreira V, Lewandowski A, et al..Normal variation of magnetic resonance T1 relaxation times in the human population at 1.5T using ShMOLLI.J Cardiovasc Magn Reson.2013;15:13.
20. Piechnik SK, Ferreira VM, Dall’Armellina E, et al..Shortened modified look-locker inversion recovery (ShMOLLI) for clinical myocardial T1-mapping at 1.5 and 3 T within a 9 heartbeat breathhold.J Cardiovasc Magn Reson.2010;12:69.
21. Liu CY, Liu YC, Wu C, et al..Evaluation of age-related interstitial myocardial fibrosis with cardiac magnetic resonance contrast-enhanced T1 mapping: MESA (multi-ethnic study of atherosclerosis).J Am Coll Cardiol.2013;62:1280–1287.
22. Messroghli DR, Walters K, Plein S, et al..Myocardial T1 mapping: application to patients with acute and chronic myocardial infarction.Magn Reson Med.2007;58:34–40.
23. Chow K, Flewitt JA, Pagano J, et al..T2-dependent errors in MOLLI T1 values: simulations, phantoms, and in-vivo studies.J Cardiovasc Magn Reson.2012;14suppl 1P281.
24. Robson MD, Piechnik SK, Tunnicliffe EM, et al..T1 measurements in the human myocardium: the effects of magnetization transfer on the SASHA and MOLLI sequences.Magn Reson Med.2013[Epub ahead of print].
25. White SK, Sado DM, Flett AS, et al..Characterising the myocardial interstitial space: the clinical relevance of non-invasive imaging.Heart.2012;98:773–779.
26. Ellims A, Iles L, Ling L-h, et al..Diffuse myocardial fibrosis in hypertrophic cardiomyopathy can be identified by cardiovascular magnetic resonance, and is associated with left ventricular diastolic dysfunction.J Cardiovasc Magn Reson.2012;14:76.
27. Iles L, Pfluger H, Phrommintikul A, et al..Evaluation of diffuse myocardial fibrosis in heart failure with cardiac magnetic resonance contrast-enhanced T1 mapping.J Am Coll Cardiol.2008;52:1574–1580.
28. Maceira AM, Prasad SK, Hawkins PN, et al..Cardiovascular magnetic resonance and prognosis in cardiac amyloidosis.J Cardiovasc Magn Reson.2008;10
29. Sparrow P, Messroghli DR, Reid S, et al..Myocardial T1 mapping for detection of left ventricular myocardial fibrosis in chronic aortic regurgitation: pilot study.Am J Roentgenol.2006;187:W630–W635.
30. Kawel N, Nacif M, Zavodni A, et al..T1 mapping of the myocardium: Intra-individual assessment of post-contrast T1 time evolution and extracellular volume fraction at 3T for Gd-DTPA and Gd-BOPTA.J Cardiovasc Magn Reson.2012;14:26.
31. Miller CA, Naish JH, Bishop P, et al..Comprehensive validation of cardiovascular magnetic resonance techniques for the assessment of myocardial extracellular volume.Circ Cardiovasc Imaging.2013;6:373–383.
32. White SK, Sado DM, Fontana M, et al..T1 mapping for myocardial extracellular volume measurement by CMR: bolus only versus primed infusion technique.JACC Cardiovasc Imaging.2013;6:955–962.
33. Flett AS, Hayward MP, Ashworth MT, et al..Equilibrium contrast cardiovascular magnetic resonance for the measurement of diffuse myocardial fibrosis: preliminary validation in humans.Circulation.2010;122:138–144.
34. Fontana M, White S, Banypersad S, et al..Comparison of T1 mapping techniques for ECV quantification. Histological validation and reproducibility of ShMOLLI versus multibreath-hold T1 quantification equilibrium contrast CMR.J Cardiovasc Magn Reson.2012;14:88.
35. Coelho-Filho OR, Mongeon FP, Mitchell R, et al..Role of transcytolemmal water-exchange in magnetic resonance measurements of diffuse myocardial fibrosis in hypertensive heart disease.Circ Cardiovasc Imaging.2013;6:134–141.
36. Messroghli D, Greiser A, Frohlich M, et al..Optimization and validation of a fully-integrated pulse sequence for modified look-locker inversion-recovery (MOLLI) T1 mapping of the heart.J Magn Reson Imaging.2007;26:1081–1086.
37. Ferreira V, Piechnik S, Dall’Armellina E, et al..T1-mapping for the diagnosis of acute myocarditis using cardiovascular magnetic resonance — comparison to T2-weighted and late gadolinium enhanced imaging.JACC Cardiovasc Imaging.2013;6:1048–1058.
38. Dass S, Suttie JJ, Piechnik SK, et al..Myocardial tissue characterization using magnetic resonance noncontrast T1 mapping in hypertrophic and dilated cardiomyopathy.Circ Cardiovasc Imaging.2012;5:726–733.
39. Puntmann VO, Voigt T, Chen Z, et al..Native T1 mapping in differentiation of normal myocardium from diffuse disease in hypertrophic and dilated cardiomyopathy.JACC Cardiovasc Imaging.2013;6:475–484.
40. Karamitsos TD, Piechnik SK, Banypersad SM, et al..Noncontrast T1 mapping for the diagnosis of cardiac amyloidosis.JACC Cardiovasc Imaging.2013;6:488–497.
41. Holloway CJ, Ntusi N, Suttie J, et al..Comprehensive cardiac magnetic resonance imaging and spectroscopy reveal a high burden of myocardial disease in HIV patients.Circulation.2013;128:814–822.
42. Been M, Thomson BJ, Smith MA, et al..Myocardial involvement in systemic lupus erythematosus detected by magnetic resonance imaging.Eur Heart J.1988;9:1250–1256.
43. Puntmann VO, D’Cruz D, Smith Z, et al..Native myocardial T1 mapping by cardiovascular magnetic resonance imaging in subclinical cardiomyopathy in patients with systemic lupus erythematosus.Circ Cardiovasc Imaging.2013;6:295–301.
44. Bull S, White SK, Piechnik SK, et al..Human non-contrast T1 values and correlation with histology in diffuse fibrosis
45. Scholz TD, Martins JB, Skorton DJ.NMR relaxation times in acute myocardial infarction: relative influence of changes in tissue water and fat content.Magn Reson Med.1992;23:89–95.
46. Higgins CB, Herfkens R, Lipton MJ.Nuclear magnetic resonance imaging of acute myocardial infarction in dogs: alterations in magnetic relaxation times.Am J Cardiol.1983;52:184–188.
47. Williams ES, Kaplan JI, Thatcher F.Prolongation of proton spin lattice relaxation times in regionally ischemic tissue from dog hearts.J Nucl Med.1980;21:449–453.
48. Dall’Armellina E, Piechnik SK, Ferreira VM, et al..Cardiovascular magnetic resonance by non contrast T1-mapping allows assessment of severity of injury in acute myocardial infarction.J Cardiovasc Magn Reson.2012;14:15.
49. Ugander M, Bagi PS, Oki AJ, et al..Myocardial edema
as detected by pre-contrast T1 and T2 CMR delineates area at risk associated with acute myocardial infarction.JACC Cardiovasc Imaging.2012;5:596–603.
50. Puntmann VO, Voigt T, Chen Z, et al..Native T1 mapping in differentiation of normal myocardium from diffuse disease in hypertrophic and dilated cardiomyopathy.JACC Cardiovasc Imaging.2013;6:475–484.
51. Holloway CJ, Ntusi N, Suttie J, et al..Comprehensive cardiac magnetic resonance imaging and spectroscopy reveal a high burden of myocardial disease in HIV patients.Circulation.2013;128:814–822.
52. Puntmann VO, D’Cruz D, Smith Z, et al..Native myocardial T1 mapping by cardiovascular magnetic resonance imaging in subclinical cardiomyopathy in patients with systemic lupus erythematosus.Circ Cardiovasc Imaging.2013;6:295–301.
53. Ferreira VM, Holloway CJ, Piechnik SK, et al..Is it really fat? Ask a T1-map.Eur Heart J Cardiovasc Imaging.2013[Epub ahead of print].
54. Sado DM, White SK, Piechnik SK, et al..Native T1 lowering in iron overload and anderson fabry disease; a novel and early marker of disease.J Cardiovasc Magn Reson.2013;15suppl 1O71.
55. Won S, Davies-Venn C, Liu S, et al..Noninvasive imaging of myocardial extracellular matrix for assessment of fibrosis.Curr Opin Cardiol.2013;28:282–289.
56. Sado DM, Flett AS, Banypersad SM, et al..Cardiovascular magnetic resonance measurement of myocardial extracellular volume in health and disease.Heart.2012;98:1436–1441.
57. Kellman P, Wilson J, Xue H, et al..Extracellular volume fraction mapping in the myocardium, part 2: initial clinical experience.J Cardiovasc Magn Reson.2012;14:64.
58. Shah RV, Abbasi SA, Neilan TG, et al..Myocardial tissue remodeling in adolescent obesity.J Am Heart Assoc.2013;2:e000279.
59. Tham E, Haykowsky M, Chow K, et al..Diffuse myocardial fibrosis by T1-mapping in children with subclinical anthracycline cardiotoxicity: relationship to exercise capacity, cumulative dose and remodeling.J Cardiovasc Magn Reson.2013;15:48.
60. Wong TC, Piehler KM, Kang IA, et al..Myocardial extracellular volume fraction quantified by cardiovascular magnetic resonance is increased in diabetes and associated with mortality and incident heart failure admission.Eur Heart J.2013[Epub ahead of print].
61. Plymen CM, Sado DM, Taylor AM, et al..Diffuse myocardial fibrosis in the systemic right ventricle of patients late after mustard or senning surgery: an equilibrium contrast cardiovascular magnetic resonance study.Eur Heart J Cardiovasc Imaging.2013;14:963–968.
62. Banypersad SM, Sado DM, Flett AS, et al..Quantification of myocardial extracellular volume fraction in systemic al amyloidosis: an equilibrium contrast cardiovascular magnetic resonance study.Circ Cardiovasc Imaging.2012;6:34–39.
63. Ugander M, Oki AJ, Hsu LY, et al..Extracellular volume imaging by magnetic resonance imaging provides insights into overt and sub-clinical myocardial pathology.Eur Heart J.2012;33:1268–1278.
64. Mongeon FP, Jerosch-Herold M, Coelho-Filho OR, et al..Quantification of extracellular matrix expansion by CMR in infiltrative heart disease.JACC Cardiovasc Imaging.2012;5:897–907.
65. Broberg CS, Chugh SS, Conklin C, et al..Quantification of diffuse myocardial fibrosis and its association with myocardial dysfunction in congenital heart disease.Circ Cardiovasc Imaging.2010;3:727–734.
66. Aletras AH, Tilak GS, Natanzon A, et al..Retrospective determination of the area at risk for reperfused acute myocardial infarction with T2-weighted cardiac magnetic resonance imaging: histopathological and displacement encoding with stimulated echoes (dense) functional validations.Circulation.2006;113:1865–1870.
67. Abdel-Aty H, Cocker M, Meek C, et al..Edema
as a very early marker for acute myocardial ischemia: a cardiovascular magnetic resonance study.J Am Coll Cardiol.2009;53:1194–1201.
68. Friedrich MG, Sechtem U, Schulz-Menger J, et al..Cardiovascular magnetic resonance in myocarditis: a JACC white paper.J Am Coll Cardiol.2009;53:1475–1487.
69. Yilmaz A, Ferreira V, Klingel K, et al..Role of cardiovascular magnetic resonance imaging (CMR) in the diagnosis of acute and chronic myocarditis.Heart Fail Rev.2013;18:747–760.
70. Giri S, Chung YC, Merchant A, et al..T2 quantification for improved detection of myocardial edema
.J Cardiovasc Magn Reson.2009;11:56.
71. Tunnicliffe EM, Robson MD.Optimising acquisition parameters for myocardial T2 mapping using T2-prep at 3T.J Cardiovasc Magn Reson.2013;15suppl 1W10.
72. Thavendiranathan P, Walls M, Giri S, et al..Improved detection of myocardial involvement in acute inflammatory cardiomyopathies using T2 mapping.Circ Cardiovasc Imaging.2011;5:102–110.
73. von Knobelsdorff-Brenkenhoff F, Prothmann M, Dieringer M, et al..Myocardial T1 and T2 mapping at 3T: reference values, influencing factors and implications.J Cardiovasc Magn Reson.2013;15:53.
74. Usman AA, Taimen K, Wasielewski M, et al..Cardiac magnetic resonance T2 mapping in the monitoring and follow-up of acute cardiac transplant rejection: a pilot study.Circ Cardiovasc Imaging.2012;5:782–790.
75. Wassmuth R, Prothmann M, Utz W, et al..Variability and homogeneity of cardiovascular magnetic resonance myocardial T2-mapping in volunteers compared to patients with edema
.J Cardiovasc Magn Reson.2013;15:27.
76. van Heeswijk RB, Hln Feliciano, Cd Bongard, et al..Free-breathing 3 T magnetic resonance T2-mapping of the heart.JACC Cardiovasc Imaging.2012;5:1231–1239.
77. Verhaert D, Thavendiranathan P, Giri S, et al..Direct T2 quantification of myocardial edema
in acute ischemic injury.JACC Cardiovasc Imaging.2011;4:269–278.