The evidence is increasing that left ventricular noncompaction cardiomyopathy as it is
currently defined does not represent a failure of compaction of pre-existing trabecular
myocardium found during embryonic development to form the compact component of the
ventricular walls. Neither is there evidence of which we are aware to favour the notion that
the entity is a return to a phenotype seen in cold-blooded animals. It is also known that when
seen in adults, the presence of excessive ventricular trabeculations does not portend a poor …