Amyloid cardiomyopathy (CA) was previously considered to be a rare disease, however, it is currently more frequently diagnosed owing to the application of rapidly developing imaging modali ties. The deposition of misfolded, insoluble proteins in the extra cellular matrix of various tissues and organs plays a key role in the pathogenesis of systemic amyloidosis. Until now, there have been over 30 different precursor proteins described which have the potential to form amyloid fibrils. On the other hand, novel emerging ATTR therapies are currently under investigation and there are numerous particles being devel oped. Gene therapy includes patisiran, a short interfering RNA (siRNA) molecule, and inotersen, an antisense oligonucleotide. Both drugs were investigated in patients with neuropathic ATTRm variants, however, the efficacy and safety of the drugs in CA has yet to be verified [15, 16, 17, 18]. Inotersen has been shown to increase the risk of adverse effects including glomerulonephritis (3%) and life‑threatening thrombocytopaenia (3%). Furthermore, tetra mer‑stabilizing therapy is becoming available. Histopathological ex amination of cardiac tissue and amyloid typing remain an available diagnostic approach for those patients who do not meet the above diagnostic criteria.