Transthyretin amyloidosis (ATTR) is a systemic disease characterized by the deposition of misfolded transthyretin (TTR) fibrils. It most commonly presents as cardiomyopathy (ATTR-CM), particularly in elderly patients with the wild-type form, whereas hereditary variants may manifest with polyneuropathy (ATTRv-PN) and/or cardiac involvement. The widespread adoption of non-invasive diagnostic pathways has increased disease recognition and facilitated the early initiation of disease-modifying therapies. Stabilizers limit dissociation of the TTR tetramer and the formation of new amyloid fibrils. Tafamidis demonstrated a benefit on mortality and cardiovascular hospitalizations in the ATTR-ACT trial and remains the treatment supported by the most robust evidence, with greater efficacy when initiated at earlier disease stages
