 Traditional thought has been that LVNC results from arrest of the normal trabecular regression and myocardial compaction that occurs during embryological development. However, this concept is challenged by reported cases of acquired LVNC, where serial echocardiograms have demonstrated a transition from a normal endocardial appearance to a hypertrabeculated LVNC phenotype. Whether this is a delayed presentation of a genetically heterogeneous cardiomyopathy or a morphological epiphenomenon shared by many phenotypically distinct cardiomyopathies, remains unknown. This irresolution is exemplified by international discordance, with the American Heart Association classifying LVNC as a genetic cardiomyopathy and the European Society of Cardiology and World Health Organisation taking the view that LVNC remains an unclassified cardiomyopathy. 