This compendium review integrates pathophysiological insights across major and rarer cardiac amyloid subtypes with nuclear imaging, contextualizing mechanisms through clinical phenotypes.
This review provides a comprehensive overview of cardiac amyloidosis pathophysiology and the central role of molecular imaging in contemporary management and risk stratification.
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 -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.
Tersalvi et al. (Fri,) conducted a review in Cardiac amyloidosis. Molecular imaging was evaluated. This compendium review integrates pathophysiological insights across major and rarer cardiac amyloid subtypes with nuclear imaging, contextualizing mechanisms through clinical phenotypes.