Abstract
Cardiac magnetic resonance (CMR) imaging has been widely used to assess myocardial perfusion and scar and is the non-invasive gold standard for identification of focal myocardial fibrosis. However, the late gadolinium enhancement technique is limited in its accuracy for absolute quantification and assessment of diffuse myocardial fibrosis by technical and pathophysiological features. CMR relaxometry, incorporating T1 mapping, has emerged as an accurate, reproducible, highly sensitive, and quantitative technique for the assessment of diffuse myocardial fibrosis in a number of disease states. We comprehensively review the physics behind CMR relaxometry, the evidence base, and the clinical applications of this emerging technique.
Highlights
Signal recovery from each myocardial voxel is acquired at different TIs following a single inversion pulse, all gated to the same cardiac phase, thereby enabling a pixel-based T1 quantification in the myocardium
Mean myocardial T1 relaxation time was significantly shorter in diabetic patients than in volunteers both at 5 (312 ± 5 vs. 361 ± 6 ms, respectively, p < 0.001) and 15 min (405 ± 6 vs. 456 ± 5 ms, respectively, p < 0.001) after gadolinium injection
Post-contrast myocardial T1 time was significantly shorter in patients with HCM compared to controls, consistent with diffuse myocardial fibrosis (498 ± 80 vs. 561 ± 47 ms, p < 0.001)
Summary
Brix et al [31] Kay and Henkelman [32] Gowland and Leach [33] Been et al [34] Gowland et al [35] Ordidge et al [36] Gowland and Mansfield [37] Freeman et al [39]. Signal recovery from each myocardial voxel is acquired at different TIs following a single inversion pulse, all gated to the same cardiac phase, thereby enabling a pixel-based T1 quantification in the myocardium. The T1 mapping with MOLLI sequence is sensitive to extremes of heart rate (bradycardia or tachycardia) [22] leading to slightly underestimation of T1 values This may be corrected though “heart rate correction” by changing in the timing of the readouts with respect to the inversion pulses at different heart rates. Pre-contrast T1 values of myocardial fibrosis (infarction scar) are significantly longer than those of normal myocardium (1,060 ± 61 vs 987 ± 34 ms) [43]. Infarction, myocarditis, and interstitial diffuse fibrosis, all have high pre-contrast T1 values when compared with normal myocardial T1 times [17, 20, 43]. These include technical challenges such as variations of T1 times at different field strength and across different vendors, and the TABLE
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