Introduction Hypertrophic cardiomyopathy (HCM) is a common myocardial disease and is the leading cause of sudden death in young individuals[1]. Although LGE can detect focal cardiac fibrosis well in HCM, it has limitations in detecting diffuse fibrosis and it suffers from contrast agent contraindication[2, 3]. Both T1 rho and native T1 map are promising tools to endogenously assess myocardial fibrosis[2-4]. However, the comparison of their exhibition in detecting myocardial fibrosis in HCM has not been reported yet. The aim of this study is to explore and further compare the feasibility of T1 rho and native T1 mapping for endogenous assessment of diffuse and focal myocardial fibrosis in patients with hypertrophic cardiomyopathy (HCM).
Methods 28 patients with HCM and 8 healthy volunteers were prospectively enrolled. All the CMR protocols were conducted in 3.0T MR system (Ingenia 3.0T, Philips Healthcare, the Netherlands). T1 rho mapping, T1 mapping, and late enhancement (LGE) imaging were in 28 patients with HCM. T1 rho mapping and T1 mapping were performed in 8 healthy volunteers. T1 rho and T1 time in each segment of left ventricle were measured according to AHA 16-segment model. All segments were graded as group 1( The ratio of LGE in each segment：<10%), group 2(LGE ratio: 10-50%) or group 3 (LGE ratio:>50%). Segmental values were compared among 3 groups. Global values of were compared among LGE positive, LGE negative HCM patients and healthy controls.
Results LGE were detected in 22 HCM patients. Among three groups of all 448 segments , significant differences were existed in T1 native time (group 1, 268 segments, 1280.5±49.0ms; group2, 148 segments, 1303.6±46.4ms; group 3, 32 segments, 1366.1±63.5ms，p<0.001) as well as in T1 rho time (group 1, 47.4±5.7ms; group2, 49.6±4.9ms; group 3, 51.8±4.4ms，p<0.001) . Among LGE positive(n=22), LGE negative(n=8) HCM patients and healthy controls(n=8), there were also significant differences in global T1 native time (LGE positive, 1300.4±40.0ms; LGE negative, 1278.0±31.7;healthy controls, 1263.4±28.8ms, p=0.04) and global T1 rho time(LGE positive, 48.6±3.2ms; LGE negative, 46.5±3.1;healthy controls, 42.3±2.9ms, p<0.001). In further pairwise analysis, the global T1 native time in LGE positive HCM patients was significantly elevated compared with healthy controls(p=0.015) and there was no significant difference between LGE negative HCM patients and healthy controls(p=0.454). On the contrary, the global T1 rho time in HCM patients was significantly elevated compared with healthy controls, regardless of LGE positive (p<0.001) or negative (p=0.018). In all segments(n=448) in patients with HCM, T1 native time has a moderate correlation with LGE ratio (Spearman r=0.383, p<0.001) whereas T1 rho time had a mild correlation (Spearman r=0.229, p<0.001). In severe LGE segments (group 3, n=32) in patients with HCM, both T1 rho time (Pearson r=0.483, p<0.006) and T1 native time (Pearson r=0.475, p<0.005) had moderate correlation with LGE ratio.
Conclusion Both T1 rho and native T1 map can endogenously evaluate the severity of the fibrosis in patients with HCM. Besides, T1 rho can distinguish HCM patients without LGE from health controls.

Acknowledgements

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