Cardiac amyloidosis: An update on nuclear cardiology in diagnosis and follow-up.

Cardiac amyloidosis (CA) is an infiltrative myocardiopathy caused by extracellular deposits of misfolded proteins, with evolution to heart failure (HF) and high mortality. The main forms are light-chain amyloidosis (AL-CA) and transthyretin amyloidosis (ATTR-CA), including the wild type and hereditary. Cardiac involvement constitutes the main prognostic factor. Scintigraphy has transformed the diagnosis by identifying ATTR-CA without biopsy by cardiac imaging with [99mTc]Tc-diphosphonates, especially with SPECT/CT, which also allows quantifying the amyloid load and thus, introducing prognostic value. Amyloid PET imaging with the new pan-amyloid Radiopharmaceuticals has expanded the diagnostic possibilities, further favoring quantification, early diagnosis and prognostic evaluation and therapeutic response. In parallel, the development of modifying therapies (TTR stabilizers, gene silencers and anti-amyloid agents) has changed the prognosis of patients with CA. This Continuing Education article describes the advances in molecular imaging and its integration with disease-modifying therapies.