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Left ventricular non-compaction (LVNC) is historically considered to be a rare form of cardiomyopathy characterized by excessive and prominent trabeculations associated with deep recesses that communicate with the ventricular cavity.1 Given that prominent trabeculations are a normal feature of the intrauterine developing myocardium, LVNC is postulated to be caused by an arrest of trabecular regression that occurs during normal embryonic development.2 Nevertheless, there has been no proof of an arrest in embryonic endomyocardial morphogenesis. Moreover, both cases of de novo acquired LVNC and cases of non-compaction disappearance have been reported in the literature,3,4 calling into question the developmental hypothesis.The diagnosis of LVNC is based on the identification of a two-layer myocardium, which is thin and compacted adjacent to the epicardium and non-compacted (NC) near the endocardium.1 However, even if frequently overlooked in the past, the inner surface of the ventricles is not smooth and prominent LV trabeculations are present even in normal hearts as shown both at post-mortem inspection5 and by imaging.6 This raises the …

Left ventricular non-compaction: troubles and traps of current imaging techniques