Original Research
Noncontrast T1 Mapping for the Diagnosis of Cardiac Amyloidosis

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Objectives

This study sought to explore the potential role of noncontrast myocardial T1 mapping for detection of cardiac involvement in patients with primary amyloid light-chain (AL) amyloidosis.

Background

Cardiac involvement carries a poor prognosis in systemic AL amyloidosis. Late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) is useful for the detection of cardiac amyloid, but characteristic LGE patterns do not always occur or they appear late in the disease. Noncontrast characterization of amyloidotic myocardium with T1 mapping may improve disease detection. Furthermore, quantitative assessment of myocardial amyloid load would be of great value.

Methods

Fifty-three AL amyloidosis patients (14 with no cardiac involvement, 11 with possible involvement, and 28 with definite cardiac involvement based on standard biomarker and echocardiographic criteria) underwent CMR (1.5-T) including noncontrast T1 mapping (shortened modified look-locker inversion recovery [ShMOLLI] sequence) and LGE imaging. These were compared with 36 healthy volunteers and 17 patients with aortic stenosis and a comparable degree of left ventricular hypertrophy as the cardiac amyloid patients.

Results

Myocardial T1 was significantly elevated in cardiac AL amyloidosis patients (1,140 ± 61 ms) compared to normal subjects (958 ± 20 ms, p < 0.001) and patients with aortic stenosis (979 ± 51 ms, p < 0.001). Myocardial T1 was increased in AL amyloid even when cardiac involvement was uncertain (1,048 ± 48 ms) or thought absent (1,009 ± 31 ms). A noncontrast myocardial T1 cutoff of 1,020 ms yielded 92% accuracy for identifying amyloid patients with possible or definite cardiac involvement. In the AL amyloidosis cohort, there were significant correlations between myocardial T1 time and indices of systolic and diastolic dysfunction.

Conclusions

Noncontrast T1 mapping has high diagnostic accuracy for detecting cardiac AL amyloidosis, correlates well with markers of systolic and diastolic dysfunction, and is potentially more sensitive for detecting early disease than LGE imaging. Elevated myocardial T1 may represent a direct marker of cardiac amyloid load. Further studies are needed to assess the prognostic significance of T1 elevation.

Key Words

amyloid
cardiovascular magnetic resonance
T1 time

Abbreviations and Acronyms

AL
amyloid light-chain
CMR
cardiac magnetic resonance
ECG
electrocardiography
LGE
late gadolinium enhancement
LV
left ventricular
ROC
receiver-operating characteristic
RV
right ventricular
ShMOLLI
shortened modified look-locker inversion recovery

Cited by (0)

Drs. Piechnik and Robson have U.S. patents pending for: 61/387,591: SKP, MDR, Systems and Methods for Shortened Look Locker Inversion Recovery (ShMOLLI) Cardiac Gated Mapping of T1, September 29, 2010, all rights sold exclusively to Siemens Medical; and U.S. coexist patent pending 61/689,067: SKP, MDR, Color Map Design Method for Immediate Assessment of the Deviation From Established Normal Population Statistics and Its Application to Cardiovascular T1 Mapping Images. Drs. Karamitsos, Piechnik, Ferreira, Robson, Myerson, and Neubauer acknowledge support from the National Institute for Health Research, Oxford Biomedical Research Centre Programme. Dr. Banypersad is funded by an investigator-led research grant from GlaxoSmithKline. Dr. Ferreira is funded by the Alberta Innovates Health Solutions Clinical Fellowship and the University of Oxford Clarendon Fund Scholarship. Dr. Neubauer has a consultancy relationship with Novartis and has received support from the Oxford British Heart Foundation Centre of Research Excellence. Dr. Moon holds a grant from GlaxoSmithKline and is funded by the Higher Education Funding Council for England. University College London Hospital and University College London received a proportion of funding from the Department of Health NIHR Biomedical Research Centres funding scheme. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.