[II-PD07-5] Native hepatic T1はフォンタン患者における肝線維症の潜在的マーカーになり得る
キーワード：Fontan palliation, liver fibrosis, native hepatic T1
Introduction: Native T1, a marker of tissue remodeling, can be initially quantified for the myocardium using T1 mapping with cardiac magnetic resonance (CMR). We hypothesized that native hepatic T1 could also be quantified in patients with Fontan palliation, and provide a means of assessing liver health.
Objective: To evaluate T1 mapping for diagnosis and grading of liver fibrosis in patients with Fontan palliation.
Methods: Using the SIEMENS MAGNETON Sola 1.5T scanner, Fontan patients prospectively underwent CMR, including native T1 mapping of the myocardium in a single short axis plane. A portion of liver was contoured to quantify T1. Hepatic native T1 was measured between comparison groups with healthy control subjects (n=9) who had previously undergone CMR imaging.
Results: 5 Fontan patients participated (mean age 11.7 ± 10.5 years, 4 [75%] female). Mean native hepatic T1 for Fontan patients was 690.6 ± 28.9 ms, and significantly higher than healthy control subjects (565.1 ± 25.3 ms, p＜0.01 by ANOVA). Among Fontan patients, native hepatic T1 strongly correlated with rate of change from myocardial T1 to hepatic T1 (hepatic T1/myocardial T1) (r=0.92), and weakly correlated with liver fibrosis marker (r=0.57 for M2BPGi, r=0.5 for type 4 collagen).
Conclusion: Native hepatic T1 can be measured by T1 mapping already obtained for myocardial T1 measurement and is significantly higher in Fontan patients compared to healthy control subjects. Native hepatic T1 may be an alternative method of following fibrosis burden, though its significance requires further study.
Objective: To evaluate T1 mapping for diagnosis and grading of liver fibrosis in patients with Fontan palliation.
Methods: Using the SIEMENS MAGNETON Sola 1.5T scanner, Fontan patients prospectively underwent CMR, including native T1 mapping of the myocardium in a single short axis plane. A portion of liver was contoured to quantify T1. Hepatic native T1 was measured between comparison groups with healthy control subjects (n=9) who had previously undergone CMR imaging.
Results: 5 Fontan patients participated (mean age 11.7 ± 10.5 years, 4 [75%] female). Mean native hepatic T1 for Fontan patients was 690.6 ± 28.9 ms, and significantly higher than healthy control subjects (565.1 ± 25.3 ms, p＜0.01 by ANOVA). Among Fontan patients, native hepatic T1 strongly correlated with rate of change from myocardial T1 to hepatic T1 (hepatic T1/myocardial T1) (r=0.92), and weakly correlated with liver fibrosis marker (r=0.57 for M2BPGi, r=0.5 for type 4 collagen).
Conclusion: Native hepatic T1 can be measured by T1 mapping already obtained for myocardial T1 measurement and is significantly higher in Fontan patients compared to healthy control subjects. Native hepatic T1 may be an alternative method of following fibrosis burden, though its significance requires further study.