Feature tracking (FT) has emerged as a promising method to quantify myocardial strain using conventional cine magnetic resonance imaging (MRI). Extracellular volume fraction (ECV) by T1 mapping enables quantification of myocardial fibrosis. To date, the correlation between FT-derived left ventricular strain and ECV has not been elucidated yet. The aim of this study was to evaluate the relationship between myocardial strain by FT and ECV by T1 mapping in patients with non-ischemic dilated cardiomyopathy (NIDCM).
A total of 57 patients with NIDCM (61 ± 12 years; 46 (81%) male)) and 15 controls (62 ± 11 years; 11 (73%) male)) were studied. Using a 1.5 T magnetic resonance scanner, pre- and post- T1 mapping images of the LV wall at the mid-ventricular level were acquired to calculate the ECV by a modified Look-Locker inversion recovery (MOLLI) sequence. The radial strain (RS), circumferential strain (CS), and longitudinal strain (LS) were assessed by the FT technique. The ECV and myocardial strain were compared using a 6-segment model at the mid-ventricular level.
The ECV and myocardial strain were evaluable in all 432 segments in 72 subjects. On a patient-based analysis, NIDCM patients had a significantly higher ECV (0.30 ± 0.07 vs. 0.28 ± 0.06, p = .007) and impaired myocardial strain than the control subjects (RS, 22.7 ± 10.3 vs. 30.3 ± 18.2, p < .01; CS, -6.47 ± 1.89 vs. -9.52 ± 5.15, p < .001; LS -10.2 ± 3.78 vs. -19.8 ± 4.30, p < .001, respectively). A significant linear correlation was found between the RS and ECV (r = -0.38, p < .001) and CS and ECV, (r = 0.38, p < .001). LS and ECV also correlated (r = 0.31, p < 0.001). On a segment-based analysis, there was a significant correlation between the ECV and RS and ECV and CS (all p values 0.80).
In patients with NIDCM, significant correlation was found between myocardial strain and ECV, suggesting the FT-derived myocardial strain might be useful as a non-invasive imaging marker for the detection of myocardial fibrosis without any contrast media.

Copyright © 2019. Published by Elsevier Inc.

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