Late gadolinium enhancement and T1 mapping for the diagnosis of cardiac amyloidosis

Abstract

To explore the role of late gadolinium enhancement (LGE) and T1 mapping for detection of cardiac amyloidosis. Nine cases of cardiac amyloidosis who had diagnosed by renal biopsy diagnosed type light-chain (AL) amyloidosis and acute heart failure suspected involvement of the heart in Tianjin First Central Hospital from May 2018 to March 2019 were enrolled, and at the same time 14 cases of non-obstructive hypertrophic cardiomyopathy patients, 12 cases of healthy physical examination at the same period were enrolled as the control. All patients underwent Philips 3.0-T including plain scan as cine, T2WI, native T1 mapping and enhanced scan as perfusion, LGE imaging, post T1 mapping. For LGE cardiac magnetic resonance imaging (CMRI), a bolus of 0.1 mL/kg of gadolinium-based contrast followed by a 20 mL saline flush was administered. After a 7-minutes delay, ECG-gated images were acquired in 3 long-axis and a stack of short-axis slices identical to those of cine images using a breath-hold gradient recalled echo phase-sensitive or magnitude only inversion recovery sequence. LGE and T1 mapping CMRI observation, including cardiac function index [left ventricle end-diastolic volume (LVEDV), left ventricle end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), valvular regurgitation], cardiac morphological index [including left ventricular wall thickness, left ventricular weight (LVM)], myocardial histological characteristics and markers N-terminal pro-brain natriuretic peptide (NT-proBNP) and accompanying signs (including pericardial effusion, pleural effusion) were performed. The predominant LGE pattern in amyloidosis was diffuse left ventricular sub endocardial enhancement (3/9), diffuse in left ventricular wall enhancement (3/9), and transmural delayed enhancement in left ventricular (2/9) and non-typical delayed enhancement (1/9). Myocardial T1 was significantly elevated in cardiac AL amyloidosis patients compared to normal subjects and hypertrophic cardiomyopathy (ms: 1 497.3±22.0 vs. 1 273.3±30.1, 1 329.3±42.6, both P < 0.05). Myocardial T1 was increased in AL amyloid before LGE. A post-contrast myocardial T1 was significantly elevated in cardiac AL amyloidosis patients compared to normal subjects and hypertrophic cardiomyopathy (ms: 476.7±44.2 vs. 516.1±41.5, 569.9±12.3, both P > 0.05). Three of 9 amyloidosis patients with review images showing T1 value and cardiac function was no significantly different with the first check (ms: 1 484.8±6.5 vs. 1 497.3±22.0, P = 0.11). One-stop CMRI can improve the diagnosis of cardiac amyloidosis, LGE can display the myocardial scarring and fibrosis, and T1 mapping is sensitive to myocardial edema and diffuse fibrosis. LGE and T1 mapping can improve the diagnostic accuracy, which is very meaningful for diagnosis and follow-up of patients.