Year: 2026
Type: review
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.
Source: Journal of Nuclear Cardiology
Institutions: Mayo Clinic, Karolinska Institutet, Stockholm South General Hospital, Azienda Socio Sanitaria Territoriale degli Spedali Civili di Brescia, University of Brescia, Indiana University Indianapolis, Indiana University School of Medicine, Indiana University – Purdue University Indianapolis, University Hospital Zurich, Spanish National Centre for Cardiovascular Research, Centro de Investigación en Red en Enfermedades Cardiovasculares, Hospital Universitario Puerta de Hierro Majadahonda, The Royal Free Hospital, University College London, Cleveland Clinic, Columbia University Irving Medical Center, Boston University, Boston Medical Center
Language: English
Subfield: Internal Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $4,190
Funder: Pfizer
OpenAlex ID: W7161281615