Diagnostic Value of LGE and T1 mapping in Multiple Myeloma patients’heart

doi:10.21203/rs.3.rs-3147494/v1

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Research Article

Diagnostic Value of LGE and T1 mapping in Multiple Myeloma patients’heart

https://doi.org/10.21203/rs.3.rs-3147494/v1

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Journal Publication

published 27 Apr, 2024

Read the published version in BMC Cardiovascular Disorders →

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Background

Unidentified heart failure occurs in patients with multiple myeloma when their heart was involved. CMR with late gadolinium enhancement (LGE) and T1 mapping can identify myocardial amyloid infiltrations.

Purpose

To explore the role of CMR with late gadolinium enhancement (LGE) and T1 mapping for detection of multiple myeloma patients’heart.

Material and Methods

A total of 16 MM patients with above underwent CMR (3.0-T) with T1 mapping (pre-contrast and post-contrast) and LGE imaging. In addition, 26 patients with non-obstructive hypertrophic cardiomyopathy and 26 healthy volunteers were compared to age- and sex-matched healthy controls without a history of cardiac disease, diabetes mellitus, or normal in CMR. All statistical analyses were performed using the statistical software GraphPad Prism. The measurement data were represented by median (X) and single sample T test was adopted. Enumeration data were represented by examples and tested was adopted. All tests were two-sided, and P values < 0.05 were considered statistically significant.

Results

In MM group, LVEF was lower than healthy controls and higher than that of non-obstructive hypertrophic cardiomyopathy group, but without statistically significant difference ((%: 49.1 ± 17.5 vs. 55.6 ± 10.3、40.4 ± 15.6, all P > 0.05). Native T1 values of MM group were obviously higher than those of healthy controls and non-obstructive hypertrophic cardiomyopathy group (ms:1462.0 ± 71.3vs. 1269.3 ± 42.3、1324.0 ± 45.1, all P < 0.05). 16 cases (100%) in MM group all had LGE.

Conclusion

LGE joint T1 mapping examination can improve diagnostic accuracy and is extremely meaningful for patient diagnosis and follow-up.

Cardiovascular magnetic resonance

Late gadolinium enhancement

T1 mapping

heart failure

multiple myeloma

Multiple myeloma has various clinical manifestations, including amyloidosis, acute heart failure will occur when involving the heart, early diagnosis of wheather myocardial was involved is important. Amyloidosis is a rare diverse condition caused by the pathologic extracellular deposition of abnormal insoluble proteins throughout the body. It may exist as a primary disease or, more commonly, may be secondary to a wide array of pathologic conditions ranging from chronic infection or inflammation to malignancy. Hereditary forms also exist. Based on the structure of protein deposits, over two dozen subtypes of amyloidosis have been described, with light-chain (AL) and transthyretin (ATTR) being the most common subtypes, and often presents as a challenging diagnostic dilemma(1, 2). A single organ or multiple organ systems may be affected. In the chest, the lungs, mediastinum, pleura, and heart may be involved(3). Approximately 50% of patients with AL amyloidosis develop cardiac involvement(4), in contrast to only approximately 2% of patients with AA amyloidosis(5). Cardiac amyloidosis (CA) is a challenging and underdiagnosed cause of heart failure(6, 7). Cardiac magnetic resonance (CMR) imaging has grown rapidly in clinical application over the past several decades, and numerous clinical and experimental studies have validated CMR imaging as a useful noninvasive tool for diagnosing and managing cardiovascular disease. CMR imaging now plays a pivotal role in cardiac morphologic and functional assessment and tissue characterization, allowing for evaluating various pathologic conditions ranging from myocardial infarction and ischemic or non-ischemic cardiomyopathy to cardiac involvement in systemic diseases such as amyloidosis and sarcoidosis. CMR with late gadolinium enhancement (LGE) identifies myocardial amyloid infiltration as a characteristic pattern of global sub-endocardial or transmural LGE coupled with abnormal myocardial and blood-pool gadolinium kinetics(8–12). Traditional LGE MR images are most useful for evaluating focal diseases since they allow for the use of normal myocardium as a standard of reference and the detection of an enhancement pattern. If gadolinium uptake is uniform, diffuse fibrosis may go undetected on qualitative images; T1 mapping is sensitive to myocardial edema and diffuse fibrosis. To our knowledge, T1 mapping for diffuse fibrosis quantification has been validated relative to histologic findings only in small numbers of patients with hypertrophic cardiomyopathy, aortic valve disease(13, 14), and in the postoperative cardiac transplantation setting(15). Native T1 mapping has emerged as a potentially useful diagnostic CMR technique for the identification of both AL and ATTR CA without recourse to contrast agents(16, 17). Abnormal native T1 mapping and ECV were associated with higher all-cause mortality in CA. Therefore, both quantitative techniques are valuable and should be considered in all patients undergoing MRI with suspected or confirmed CA(18, 19). This study aims to determine the value of CMR in diagnosing and evaluating myocardial amyloidosis in MM patients by comparing differences between non-cardiac history, non-obstructive hypertrophic cardiomyopathy using LGE and T1 mapping.

Study population

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 above (M:F = 9:7; mean age, 60.0 ± 8.9 years) underwent CMR (3.0-T) with T1 mapping (pre-contrast and post-contrast) and LGE imaging. In addition, 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) were compared to age- and sex-matched healthy controls without a history of cardiac disease, diabetes mellitus, or normal in CMR. Every participant agreed to undergo a hematocrit blood test within 24 h before CMR scan.confirming that informed consent was obtained from all subjects and/or their legal guardian(s).

Follow-up

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.

CMR acquisition

CMR was performed on a 3T system (Ingenia, Philips Medical Systems, Best, the Netherlands). The body coil was used for radiofrequency transmission with 16 elements for reception. 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°.

T1 mapping was performed for all participants in 3 layers with basel- ventricular, mid-ventricular and apex-ventricular short-axis view. For the pre-contrast, MOLLI 5s(3s)3s 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 (10–15) min after the ejection. 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°.

LGE images were performed along the long-axis and short-axis views using phase sensitive inversion recovery about (10–11) min after the ejection. 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, measured at that time.

Image analysis

CMR analysis was performed in balanced steady-state-free-precession cine images in Intellispace Portal 7. The endocardial and epicardial borders of LV were manually sketched in the end-diastolic and end-systolic phases, respectively, and trabeculations were all excluded from endocardial borders.

Observers to label: (1) cardiac function: LVEDV and LVESV, LVEF and valvular regurgitation; (2) cardiac morphological indicators: left ventricular wall thickness and left ventricular mass (LVM); (3) histologic 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) myocardial markers and accompanying signs such as N terminal brain natriuretic peptide precursor (NT - proBNP), pericardial effusion, and pleural effusion.

Statistics

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:

ECV = (1 − hematocrit) × [(1/ myo post T1-1 /myo native T1)/(1/blood post T1-1/ blood native T1)]

To determine T1 values for the three groups, pre-T1 mapping was performed of 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 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.

Joint inspection of the cardiac function indexes (Table 1): in MM group, LVEF was lower than healthy controls (but still within the normal range) and higher than that of non-obstructive hypertrophic cardiomyopathy group, but without statistically significant difference ((%: 49.1 ± 17.5 vs. 55.6 ± 10.3、40.4 ± 15.6, all P > 0.05); however, LVEDV and LVESV were significantly lower than healthy controls and non-obstructive hypertrophic cardiomyopathy group, exhibiting statistically significant difference [LVEDV(ml/m²): 100.6 ± 33.8 vs.117.5 ± 25.9、156.7 ± 49.8, LVESV(ml/m²): 53.6 ± 25.7 vs. 52.7 ± 16.3、96.7 ± 50.3, all P < 0.05]. Native T1 values of MM group were obviously higher than those of healthy controls and non-obstructive hypertrophic cardiomyopathy group (ms: 1462.0 ± 71.3vs. 1269.3 ± 42.3、1324.0 ± 45.1, all P < 0.05); and enhanced T1 values were less than those of the above two groups, but without statistically significant difference (ms༚479.3 ± 66.7 vs. 516.0 ± 61.1、499.0 ± 65.9,all P > 0.05). LVM in MM group was obviously higher than that of healthy controls but less than that of non-obstructive hypertrophic cardiomyopathy group (g: 156.9 ± 50.6vs. 109.0 ± 27.0、232.4 ± 89.8, all P < 0.05).

Cardiac morphological indexes of MRI results (Table 1): in MM group, 14 cases(87.5%) of patients had left ventricular wall thickening (diastolic ending the thickest > 12 mm), including nine cases (56.2%) with right ventricular wall thickening together; all 26 (100%) patients of non-obstructive hypertrophic cardiomyopathy had left ventricular wall thickening, but none had right ventricular wall thickening.

Myocardial histology characteristics (Table 1): LGE can be characterized by left ventricular patchy reinforcement, improved endocardium under strip, improved endocardium, and occasionally can be extended to the epicardial region and not the typical abnormal delay late when amyloidosis involves the myocardium. A total of 16 cases (100%) in MM group all had LGE, including six cases of left ventricular wall patchy reinforcement, six cases of left ventricular endocardial diffuse strengthening, and three cases of intensive endocardial limitations; one case was not typical abnormal delay later reinforcement; 19/26 cases (73.1%) in non-obstructive hypertrophic cardiomyopathy group had LGE, but the region strengthened is segmental myocardial, confined to significantly different with MM’s cardiac amyloidosis strengthening characteristics; and 26 cases of healthy controls had no LGE. There are 6/16 cases (37.5%) and 9/16 cases (56.3%) with pericardial effusion and pleural effusion in MM group.

Adolinium clearance time in blood pools is approximately 5min. Due to abnormal protein deposition, amyloidosis and blood pool clear faster, enhanced T1 values of MM group were obviously lower than those of healthy controls, but without statistically significant difference (ms: 479.3 ± 66.7vs. 516.0 ± 61.1, P > 0.05).

Table 1

MM and non-obstructive hypertrophic cardiomyopathy patients MRI results compared
	Healthy controls(n = 26)	Hypertrophic cardiomyopathy(n = 26)	Multiple myeloma (n = 16)	P₁	P₂
age(years)	49.9 ± 18.0	51.7 ± 12.4	60.0 ± 8.9	0.18	0.36
gender(M/F)	16/10	16/10	9/7	0.73	0.73
LVEDV(ml/m²)	117.5 ± 25.9	156.7 ± 49.8	100.6 ± 33.8	0.338	0.001
LVESV(ml/m²)	52.7 ± 16.3	96.7 ± 50.3	53.6 ± 25.7	0.995	0.004
LVEF(%)	55.6 ± 10.3	40.4 ± 15.6	49.1 ± 17.5	0.314	0.206
LVM(g)	109.0 ± 27.0	232.4 ± 89.8	156.9 ± 50.6	0.05	0.005
LVPWT(>12mm)	-	26(100%)	14(87.5%)	< 0.001	0.06
Valvular regurgitation	-	21(80.7%)	16(100%)	< 0.001	0.138
Perfusion defects	-	-	7(43.5%)	0.002	0.002
LGE	-	19(73.1%)	16(100%)	< 0.001	0.02
Native T1	1269.3 ± 42.3	1324.0 ± 45.1	1462.0 ± 71.3	< 0.001	< 0.001
Enhanced T1	516.0 ± 61.1	499.0 ± 65.9	479.3 ± 66.7	0.428	0.825
ECV(%)	27.7 ± 2.3	29.2 ± 4.3	45.7 ± 6.7	< 0.001	< 0.001
Pericardial effusion	-	-	6(37.5%)	< 0.001	< 0.001
Pleural effusion		-	9(56.3%)	< 0.001	< 0.001

LVEDV: left ventricular diastolic final volume; LVESV༚left ventricular systolic final volume; LVEF༚left ventricular ejection fraction; LVM༚the quality of the left ventricle; LVPWT༚Left ventricular wall thickening; ECV: extracellular volume;

ROC curve analysis of native T1 value between MM group with healthy controls group and non-obstructive hypertrophic cardiomyopathy group showed that the cut-off value of T1 were 1345 ms and 1348 ms, the areas under the curve were 1.0, P < 0.001and 0.91, P = 0.001, the specificity were 100% and 100%, and the sensitivity were 100% and 61.6% (Fig. 1), respectively. At the same time, T1 value increased and LVEF decreased, while LV quality increased.

Considering the systemic amyloidosis sedimentary characteristics and renal function in patients with conditions, there are three MM patients with amyloidosis involving myocardium for review after treatment, are one period after chemotherapy CMR scan interval (two months), native T1 value is (1484.8 ± 6.5) ms after chemotherapy and (1462.0 ± 71.3) ms before chemotherapy, there was no statistically significant difference (P = 0.12), showed no obvious progress in amyloidosis involving myocardium. The images characteristics between MM group with healthy controls group and non-obstructive hypertrophic cardiomyopathy group showed in Fig. 2.

Myocardial thickening is a significant symptom of amyloidosis involving myocardium, characterized by diffuse thickening of the left ventricular wall, most frequently occurring when the left ventricular wall thickening of unexplained > 12 mm in the presence of suspected myocardial involvement(20). In the study of nine MM patients with amyloidosis involving myocardium, the left ventricular wall thickening (At the end of diastolic, thickest place > 12 mm) occurred, and when heart muscle shun drops diastolic dysfunction occurs, later can cause shrinkage function obstruction, and part may be accompanied by pericardium and (or) pleural effusion. By including six cases with pericardial effusion and nine cases with pleural effusion, the emergence of effusion may be caused by cardiac insufficiency or amyloid deposition in pericardium or pleural effusion(21). By amyloid deposition in the left ventricular wall, delayed enhancement imaging of the left ventricular wall thickness in the initial morphological change, fat suppression sequences, and T2WI images, observers can delay strengthening of the endocardium, endocardial fat, and pericardial effusion.

The typical LGE model of amyloidosis involving myocardium can be characterized by diffuse or under endocardium or through a wall of delayed reinforcement(22). In this study, nine MM cases with myocardial lake powder samples represent delayed reinforcement. Although late ischemic heart disease may also have similar performance, this can be proved to be associated with vascular distribution and myocardial thin rather than myocardial thickening. Although research has demonstrated a positive correlation between LGE myocardial enhanced imaging features and amyloid deposits, amyloidosis involving myocardium can emerge during early delayed reinforcement(23). In addition to the performance of delayed myocardial reinforcement, blood pool gadolinium (Gd) early clearance in amyloidosis patients is more obvious. Therefore, after injection of contrast medium 10 ~ 15 min, amyloidosis patients have a significantly lower signal intensity in blood pool than healthy subjects, signaling a much earlier reduction in blood flow to the heart cavity. This phenomenon is because systemic Gd contrast agents were stranded in the whole-body tissue amyloid(24). Amyloidosis involving myocardium was a gradual accumulation of amyloid in the myocardial interstitium material, increasing ventricular wall thickness and quality and eventually causing diastolic and systolic function disorders(25).

T1 mapping can detect cardiac involvement of amyloidosis and evaluate amyloid deposition in the heart. The enhanced T1 relaxation time of T1 mapping measurement of heart muscle before use can evaluate myocardial edema and fibrosis caused by interstitial expansion. Enhanced T1 mapping to distinguish whether T1 values for amyloidosis involving myocardium is also very meaningful. Krombach et al.(24), in a quantitative study of T1, demonstrated that when amyloidosis involving myocardium occurs, T1 values significantly increase. Although the impact of T1WI scan on myocardial signal level is difficult to distinguish, prompt T1 values of quantitative diagnosis, T1 threshold 1 273 ms or higher (1.5 T) indicate amyloidosis, diagnostic accuracy, the highest sensitivity of 84%, the specific degree of 89%, and enhanced T1 mapping of myocardial T1 values significantly lower than normal. Ferreira(26) used T1 mapping technologies such as computing and different segmental myocardial blood pools to boost T1 values before and after calibration, hematocrit, and calculating ECV cell content (ICV), in addition to amyloid and myocardial cell volume.

Amyloidosis involving myocardium in MM patients has a worse prognosis. Although the biopsy is the "gold standard" for diagnosing amyloidosis involving myocardium, it could not follow up on patients following treatment. CMR, except for early diagnosis and differential diagnosis, may be used to determine the severity of myocardial amyloid sex by assessing the extent of ventricular wall thickness, LVM, and delay to strengthen, as well as for follow-up to evaluate the effect of treatment and noninvasive examination(11, 27, 28). Following evaluation, T1 mapping and LGE in treating patients have been demonstrated to significantly improve T1 mapping before to diagnosis(29).

CMR examination revealed that myocardial hypertrophy, cardiac diastolic function obstruction, under the endocardium (patchy, diffuse, or through the wall), T1 values increase, blood pool contrast agent expurgation rate is faster and pericardial effusion and pleural effusions are present, which can improve diagnostic efficacy. LGE joint T1 mapping examination can improve diagnostic accuracy and is extremely meaningful for patient diagnosis and follow-up.

multiple myeloma (MM) ; Cardiac magnetic resonance (CMR); Cardiac amyloidosis (CA); late gadolinium enhancement (LGE); hypertrophic cardiomyopathy(HCM); healthy control(HC); LVEF; left ventricular diastolic final volume(LVEDV); left ventricular systolic final volume(LVESV); left ventricular mass (LVM);extracellular volume(ECV)

Ethical Approval and Consent to participate :

A statement to confirm that all methods were carried out in accordance with relevant guidelines and regulations(declaration of helsinki)

A statement to confirm that all experimental protocols were approved by Tianjin First Center Hospital licensing committee.

confirming that informed consent was obtained from all subjects and/or their legal guardian(s).

Institutional Review Board approval was obtained.

Review date: Aug,8th,2020

Review number:2020N077KY

Consent for publication:

Written consents were obtained from each patient to publishing their pathological images as represent Figures.

Availability of data and materials:

The datasets used during the current study are available from the corresponding author on reasonable request.

Conflict of Interest:

The authors have declared that no competing interests exist.

Funding:

This study was supported by Tianjin Health Commission Science and Technology Talent Cultivation Project(RC20184)，Tianjin Health Commission Science and Technology Key Project（ZD20002）

Tianjin Key Medical Discipline (Specialty) Construction Project, Tianjin Institute of imaging medicine, and the Natural Scientific Foundation of Tianjin (21JCQNJC01640).

Authors' contributions:

Qian Cui wrote this paper; Jing Yu and Yang Liu participated in the data collection and clinical analysis; Xihong Ge and Guangfeng Gao assisted the data analysis; Qiang He made diagnosis of myocardial lesions in patients;Wen Shen designed this study and revised the paper.

Acknowledgements:

Not applicable.

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No competing interests reported.

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Diagnostic Value of LGE and T1 mapping in Multiple Myeloma patients’heart

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Abstract

Background

Purpose

Material and Methods

Results

Conclusion

Figures

Introduction

Material and Methods

Study population

Follow-up

CMR acquisition

Image analysis

Statistics

Results

Discussion

Conclusion

Abbreviations

Declarations

References

Additional Declarations

Status:

Journal Publication

Version 1