IJCS | Volume 32, Nº2, March/April 2019

184 Figure 6 - (A) Modified lock-locker inversion recovery (MOLLI) T1 mapping on the short axis showing the myocardium (green) and the blood (blue). (B) T1 relaxation curve (482 ms for the myocardium). Ribeiro et al. CMR and amyloidosis Int J Cardiovasc Sci. 2019;32(2)177-189 Review Article by magnetic resonance, including measurements of the T2 (edema) and T2* (iron deposition) and T1 mapping, focusing on non-invasive quantification of diffuse myocardial fibrosis. The most used sequence for T1 mapping quantification is the modified lock-locker inversion recovery (MOLLI) (Figure 6). 44-51 With technological advances in the context of amyloidosis or even infiltrative diseases, the use of ECV expansion and T1 mapping has been consolidated in the diagnosis and follow-up of patients with myocardial interstitial disease caused by increased amyloid deposition or fibrosis. T1 mapping transforms a physical principle of magnetic resonance into a quantifiable number (expressed in milliseconds) in an image. T1 relaxation time is the measure of how quickly the longitudinal magnetization component recovers to its equilibrium state. In the T1 mapping technique, measurements of T1 relaxation with and without contrast can be obtained by a simple software that directly defines a region of interest within the myocardium, generating pre- and post-contrast administration values in milliseconds. Amyloid deposition increases T1 in the pre-contrast phase and reduces T1 in the post-contrast phase due to increased extracellular space by the amyloid infiltration. 44-51 It has demonstrated that T1 mapping without contrast can identify amyloid deposits with a T1 of approximately 1,140 ± 61 ms. 29 In post-contrast studies, the cut-off value demonstrated to have a worse prognosis was 565 ms when combined with a pre- contrast value greater than 1,044 ms. 52 In addition, the use of pre- and post-contrast T1 mapping enables the calculation of the ECV fraction by the relationship between relaxation fractions of the cardiac muscle and the blood, corrected by hematocrit: (ΔR1 myocardium / ΔR1 blood )*(1 – Ht) Normal ECV in healthy volunteers is 27 ± 3%. 46,49 These made the assessment of interstitial fibrosis or subclinical amyloid deposition by T1 mapping possible, even in situations of negative delayed enhancement magnetic resonance imaging. T1 time is decreased in the presence of fibrosis (Figure 7), making this map and powerful tool for quantification of ECV expansion and fibrosis. T1 mapping has been validated by endomyocardial biopsies in patients with non-ischemic heart diseases, referred for cardiac transplantation. 51 The measurement of the ECV fraction determines, in percentage, areas of possible fibrosis not yet detected by delayed enhancement technique. 52-54