Published: 16 May 2022
Author(s): Sebastian Göbel, Lukas Hobohm, Alexander Desuki, Tommaso Gori, Thomas Münzel, Rapezzi Claudio, Philip Wenzel, Karsten Keller
Issue: August 2022
Section: Original article

Amyloidosis is a multi-systemic disease resulting from deposition of misfolded proteins as insoluble fibrils in the interstitium of affected organs, subsequently leading to organ failure. Cardiac involvement in amyloidosis is common [1] and amyloid fibrils can deposit in several cardiac structures, including coronary arteries, ventricles, atria and heart valves [2,3]. Although more than 30 proteins can form amyloid fibrils, cardiac amyloidosis is typically attributable to misfolded transthyretin (ATTR) or immunoglobulin light chain (AL) aggregation [4].

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