Background: In vivo mechanisms of amyloid clearance and cardiac tissue damage in cardiac amyloidosis are not well understood.
Objectives: We aimed to define and quantify the amyloid plaque proteome in cardiac transthyretin amyloidosis (ATTR) and light chain amyloidosis (AL) and identify associations with patient characteristics and outcomes.
Methods: A proteomics approach was used to identify all proteins in cardiac amyloid plaques, and to compare both normal and diseased controls.