Abstract
The use of cardiac magnetic resonance (CMR) for accurate morphological assessment of cardiomyopathies is well described. CMR tissue characterization with late gadolinium enhancement and parametric mapping is highly promising in differentiating key etiologies of left ventricular hypertrophy, diagnosing cardiac involvement in systemic amyloidosis, detecting early disease, and tracking changes over time, as well as providing valuable prognostic information. This review focuses on the typical imaging findings in cardiac amyloidosis by CMR, highlighting its potentials with respect to traditional imaging techniques. Furthermore, the diagnostic and prognostic role of CMR parameters and the future perspectives related to the newest applications are addressed.
Highlights
Amyloidosis is caused by aggregation and deposition of misfolded autologous proteins in the extracellular space of several organs
cardiac magnetic resonance (CMR) confirmed the echocardiographic finding of a global reduction of longitudinal strain (LS), with a “relative apical sparing” pattern, providing mechanistic insights: the concomitant presence of a base-to-apex gradient of late gadolinium enhancement (LGE) burden suggested that the regional strain gradient may be related to the burden of amyloid deposition[15]
Besides a more prevalent sub-endocardial LGE in AL than ATTR, AL patients present a greater elevation of native T1 and lower extracellular volume (ECV), suggesting that the amyloid burden might be higher in ATTR; higher native T1 with smaller amyloid burden in AL points to additional pathologic processes, and the most likely is edema related to light chain toxicity or rapid deposition[35,36,37]
Summary
Amyloidosis is caused by aggregation and deposition of misfolded autologous proteins in the extracellular space of several organs. CMR confirmed the echocardiographic finding of a global reduction of LS, with a “relative apical sparing” pattern, providing mechanistic insights: the concomitant presence of a base-to-apex gradient of late gadolinium enhancement (LGE) burden suggested that the regional strain gradient may be related to the burden of amyloid deposition[15].
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