Published: 28 May 2020
Author(s): Alberto Aimo, Giuseppe Vergaro, Vincenzo Castiglione, Claudio Rapezzi, Michele Emdin
Section: Original article

Amyloidosis is a systemic disease characterized by extracellular deposition of insoluble fibrils, deriving from proteins encoded by mutated genes or normal, misfolded proteins [1,2]. Previously considered a very rare condition, amyloidosis is increasingly recognized as an important cause of cardiac disease [3]. Cardiac involvement is common in both immunoglobulin light-chain (AL) and transthyretin amyloidosis (ATTR), and is a major determinant of clinical presentation and outcome; it may manifest with left ventricular (LV) pseudohypertrophy and/or heart failure with preserved or mid-range ejection fraction (HFpEF/HFmrEF), possibly evolving towards systolic dysfunction, and sometimes accompanied by conduction disturbances or arrhythmias [1,2].


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