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Systemic amyloidosis still remains a challenging and probably underdiagnosed disease.1
The three most frequent types of systemic amyloidosis are (i) the acquired monoclonal immunoglobulin light chain amyloidosis (AL), characterised by clonal plasma cells in the bone marrow that produce the immunoglobulin lights chains of the fibrillary deposits; (ii) the hereditary, transthyretin (TTR)-related form (ATTR), which can be caused by 100 mutations of TTR, a transport protein synthesised mainly by the liver; and (iii) the wild-type (non-mutant) TTR-related amyloidosis called systemic ‘senile’ amyloidosis (SSA), which affects mainly the hearts of elderly men.1 ,2
Pozo et al3 focus on the problem of LV remodelling and on the type of distribution of the ‘hypertrophy’ in patients with cardiac amyloidosis (CA). The concepts of ‘LV remodelling’ and ‘LV geometry’ have been elaborated in the last 20 years mainly related to coronary heart disease, hypertensive heart disease4 and valvular heart disease. Regarding hypertensive heart disease, a spectrum of LVH exists ranging from concentric LV hypertrophy (LVH), characterised by increased LV mass and increased ratio of the LV wall thickness to diastolic diameter (relative wall thickness, RWT), …
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