J Nucl Cardiol. 2026 May;59S:102723. doi: 10.1016/j.nuclcard.2026.102723. Epub 2026 May 15.
ABSTRACT
Cardiac amyloidosis (CA) has transitioned from a rare, frequently fatal disease to an increasingly recognized cause of heart failure, driven by heightened awareness, noninvasive diagnostic strategies, and the advent of disease-modifying therapies. As a result, molecular imaging has become central to contemporary management by providing signals that reflect underlying disease biology. Transthyretin CA predominantly involves progressive extracellular fibril accumulation causing myocardial stiffening, whereas light-chain CA is characterized by early myocardial dysfunction mediated by direct proteotoxic effects of circulating light chains in addition to extracellular fibril accumulation. These divergent mechanisms may underlie different behaviors of diagnostic imaging such as bone-avid scintigraphy and β-sheet-binding positron emission tomography tracers. In this compendium review, we integrate pathophysiological insights across major and rarer amyloid subtypes with nuclear imaging and contextualize these mechanisms through clinical phenotypes, red flags, and risk stratification tools.
PMID:42142944 | DOI:10.1016/j.nuclcard.2026.102723