CMR was performed in patients diagnosed with MM as having heart failure suspected myocardial involvement between May 2020 and November 2022. A total of 16 MM patients with renal biopsy as having AL amyloidosis (M:F = 9:7; mean age, 60.0 ± 8.9 years) underwent CMR (3.0-T) with T1 mapping (Native and post-contrast) and LGE imaging. In addition, We enrolled participants admitted for non-obstructive hypertrophic cardiomyopathy confirmed by cardiology department, 26 patients with non-obstructive hypertrophic cardiomyopathy (M:F = 16:10, age, 51.7 ± 12.4 years) and 26 healthy volunteers (M:F = 16:10; mean age, 49.9 ± 18.0 years) without a history of cardiac disease, diabetes mellitus, or normal in CMR were compared. Every participant agreed to undergo a hematocrit blood test within 24 h before CMR scan and informed consent was obtained from all subjects and/or their legal guardian(s).

The inclusion criteria of HCM group: a. Basal LV wall thickness ≥ 15 mm, b. ratio of septal thickness to thickness of inferior wall at midventricular level > 1.5, c. Peak gradient at LVOT or mid LV cavity < 30 mm Hg, d. no contraindications to cardiac MRI; the inclusion criteria of normal controls: without a history of cardiac disease, diabetes mellitus, or normal in CMR; the exclusion criteria of HCM group and normal controls: a. previous cardiac surgery, b. moderate to severe valvular heart disease, c. any permanent implanted device, d. Apical HCM, Obstructive HCM et. al any other cardiomyopathy. And there are 9/26 HCM paitents admission for heart failure, the LVEF is lower than 20%.

The study end-point was defined as the occurrence of cardiac death, heart transplantation, and hospitalization due to cardiovascular events. Follow-up information was obtained from in-person or telephone interview at 2-month intervals. Time to event was defined as the duration from the date of the CMR scan to an event. When had a treatment would review with native T1 mapping. The information from follow-up CMR acquisition as cardiac function (LVEDV and LVESV, LVEF and mitral valve regurgitation), cardiac morphological indicators (left ventricular wall thickness and left ventricular mass (LVM), native T1 values.

CMR was performed on a 3.0 T MRI system (Ingenia, Philips Medical Systems, Best, the Netherlands) with an 16-channel cardiac phased-array coil.

Along with long-axis planes (two-, three-, and four- chamber views), a stack of short-axis single-shot balanced standard steady-state in free-precession sequence images from apex to basal were collected. The imaging parameters were as follows: field of view, 300 mm × 300 mm; voxels, 2 mm × 2 mm × 8 mm; repetition time, (3.0–3.2) ms; echo time, (1.5–1.6) ms; sense factor, 1.8; minimum inversion time, 105 ms; and flip angle, 45°. Cine CMRI was performed using a steady-state freeprecession sequence. Fat-saturated and T2-weighted images were obtained to allow differentiation among subepicardial LGE, epicardial fat, and pericardial effusion.

T1 mapping was performed for all participants in 3 slices with basal- ventricular, mid-ventricular and apex-ventricular short-axis view. For the native T1 mapping, MOLLI 5s(3s)3 s scheme was performed. A total dose of 0.2 mmol/kg gadopentetate dimeglumine injection was administered. For post-contrast, a 4s(1s)3s(1s)2s scheme was performed [10,11,12,13,14,15] min after the injection. The imaging parameters were as follows: field of view, 320 mm × 320 mm; voxels, 2 mm × 2 mm × 8 mm; sense factor, 1.5; minimum inversion time, 105 ms; and flip angle, 20°.

First-pass myocardial perfusion were performed multi-dynamic rapid capture of the heart in less than 1 min. The relative perfusion parameters were analyzed by observing the change of signal intensity of contrast agent through myocardium. The imaging parameters were as follows: field of view, 320 mm × 320 mm; voxels, 2 mm × 2 mm × 8 mm.

LGE images were performed along the long-axis and short-axis views using phase sensitive inversion recovery about [10, 11] min after the injection. The imaging parameters were as follows: field of view, 320 mm × 320 mm; voxels, 2 mm × 2 mm × 8 mm; repetition time, (6.0–6.2) ms; echo time, (3.0–3.1) ms; and TI, adjustedat that time.

CMR analysis was performed inIntellispace Portal 7. Cine, T2WI, T1 mapping and contrast images (First-pass myocardial perfusion, LGE and post-T1mapping) were evaluated separately by 2 blinded observers. In brief, endocardial and epicardial borders were outlined on the short-axis cine images. Volumes, myocardial mass, and ejection fraction were derived by summation of epicardial and endocardial contours. For each segment, the extent of LGE was analyzed.

Observers to label: (1) cardiac function: LVEDV and LVESV, LVEF and mitral valve regurgitation; (2) cardiac morphological indicators: left ventricular wall thickness and left ventricular mass (LVM); (3) tissue features: T2 images myocardial signal, with or without perfusion defect and its position and scope, the presence of delayed enhancement and its position, shape, and scope, and the enhancement T1 values before and after, ECV; (4) accompanying signs such as pericardial effusion, and pleural effusion.

Myocardial T1 times were measured carefully in a global region of interest (ROI), including the whole ventricular wall; meanwhile, an ROI was drawn in the blood pool to measure blood pool T1 times. ECV was calculated as follows:

$$\textit=\left(1-\text\right)\times\left[\left(1/\mathrm m\mathrm y\mathrm o\;\mathrm p\mathrm o\mathrm s\mathrm t\;T1-1/\mathrm\;\mathrm\;T1\right)/\left(1/\mathrm\;\mathrm\;T1-1/\mathrm\;\mathrm\;T1\right)\right]$$

To determine T1 values for the three groups, native T1 mapping was performed and the data computed from receiver operating characteristic curves (ROC). All statistical analyses were performed using the statistical software GraphPad Prism (version 9.0; GraphPad Software, San Diego, California, USA). The measurement data were represented by median (X) and single sample T test was adopted. Enumeration data were represented by examples and Chi-tested was adopted. A comparison was made between the healthy controls group and the MM group (P1), non-obstructive hypertrophic cardiomyopathy group and the MM group (P2). All tests were two-sided, and P values < 0.05 were considered statistically significant.