Transthyretin cardiac amyloidosis (ATTR-CA) is an infiltrative cardiomyopathy caused by extracellular deposition of misfolded transthyretin (TTR) fibrils within the myocardium, leading to progressive heart failure (HF) [1]. TTR is synthesised almost exclusively by the liver; thus the liver is not only the source of the amyloidogenic precursor but also a potential target organ for amyloid deposition. Two molecular entities are recognised: hereditary or variant ATTR, produced by destabilising mutations in the TTR gene and often presenting from mid-life [2], and wild-type ATTR, which predominantly affects the elderly [1].
